BIO 122.1 LE 3

TOPIC: OSMOREGULATION

Osmoregulation

• The process by which animals maintain water and

  ion balance in cellular fluids

• Critical for cell survival, intracellular osmotic

  pressure maintenance, and solute transport

  during growth

Mechanisms of Osmoregulation in different organisms

• Freshwater fish

  • Hypertonic to the environment (blood with higher salt concentration)

  • Absorb water through mouth and gills; excretes large amounts of urine

  • Use mitochondria-rich cells in gills to absorb sal

  • Larger animals have kidneys to stabilize body fluid concentration

• Marine Fish (Saltwater fish)

  • Hypotonic to the environment (water concentration greater in the blood)

  • Limit urine, drink seawater, and expel salt through gills

• Terrestrial Animals

  • Loses water via evaporation

  • Conserves water and consumption is urgently

• Bacteria

  • Synthesize osmoprotectans under osmotic stress

  • Uses transport mechanisms to absorb electrolytes in high osmolarity

• Humans and Mammals

  • Osmotic balance maintained by kidneys (excrete excess water, electrolytes, and wastes)

  • Kidneys consist of millions of nephrons (responsible for filtration)

  • Regulates osmotic pressure across the blood

    plasma, interstitial, and intracellular fluids,

    affecting blood pressure

Earthworm Osmoregulation

• No kidneys, but possess nephridia (protonephridium and metanephridium)

• Avoid desiccation by burrowing into deep soil and emerging at night when evaporation is minimal

• Retreat deeper underground in hot/dry weather

• Retreat into enlarged burrow chambers, rolling into balls with others when the weather is cold

• Rely on coelomic fluid and permeable skin for osmoregulation

Mechanism of Osmoregulation in Earthworms

• Hyperosmotic regulation

  • When exposed to saline (super salty) environments, earthworms retain coelomic fluid and ions, preventing excessive water loss

• Hormone roles

  • Aldosterone and vasopressin-like hormones regulate water retention and ion exchange

• Coelomic Fluid

  • Buffer osmotic stress by acting as a reservoir for water and ions

  • Capacity is limited under extreme saline (super salty) conditions

Earthworm response to salinity stress

• Significant decrease in weight and volume with

  increasing salt concentrations (e.g., 0.14M and

  0.15M).

• Stable weight and volume observed at lower

  salinity levels (e.g., 0.03M) due to effective

  osmotic control.

• Hyperosmotic regulation fails at high salinity concentrations, leading to severe dehydration

• Water loss occurs to balance external hypertonic conditions

Metanephridia

• What earthworms use to osmoregulate and excrete waste

• Functions through ciliated funnels called nephrostomes (collect coelomic fluid)

• Three main types:

  • Septal Metanephridium - Processes coelomic fluid for waste removal and reabsorption of nutrients

  • Integumentary Metanephridium - Located in the body wall and plays a role in the excretion of nitrogenous waste directly through the skin. It has direct contact with the surface environment

  • Pharyngeal Metanephridium - Associated with the pharyngeal region, assisting in removing waste from the digestive tract.

Earthworm Behavior

• Rainfall

  • Earthworms thrive in moist environments.

  • After rainfall:

    • Earthworms leave the soil to avoid waterlogging.

    • Rainfall reduces soil salinity by washing away soluble salts.

• Negative Phototaxis (avoidance of light)

  • Earthworms do not have eyes but possess photoreceptor cells on their epidermis.

  • They are predisposed to avoid light, making them more active at night.

  • Adaptation mechanisms:

    • Crawling or digging underground to escape light.

    • Increased Na⁺/K⁺ pump activity and expression of the Wnk1 gene (linked to osmotic regulation).

• General adaptations

  • Setae (bristle-like hairs) on each segment and muscles help in movement through the soil.

  • Secrete mucus to aid in movement.

  • Can aestivate (enter a dormant state) during unfavorable conditions to reduce metabolic activity.

  • Increase the excretion of amino acids (e.g., urea) in the coelom to combat fluid loss.

TOPIC: BLOOD

Blood

• Comprised of 55% plasma and 45% formed elements

• Transports important substances, regulates body temperature, and works with the immune system

• Processes

  • Agglutination - red blood cells clump when the presence of an antigen interacts with its corresponding antibody

  • Clotting - clumping of platelets that plug damaged vessels to prevent blood loss and initiate healing.

• Other properties

  • Respiratory pigments - Proteins (e.g., hemoglobin) in RBCs give blood its red color and help increase its oxygen-carrying capacity.

  • Buffer action - Blood contains systems like carbonic acid and bicarbonate, which maintain the body’s pH in a narrow range (7.35–7.45), preventing the blood from becoming too acidic or alkaline.

ABO Blood Group

• Group A:

  • Antigens on RBCs: A antigen.

  • Antibodies in plasma: Anti-B antibodies (attack B antigens).

• Group B:

  • Antigens on RBCs: B antigen.

  • Antibodies in plasma: Anti-A antibodies (attack A antigens).

• Group AB:

  • Antigens on RBCs: Both A and B antigens.

  • Antibodies in plasma: None (can receive blood from all types; universal recipient).

• Group O:

  • Antigens on RBCs: None.

  • Antibodies in plasma: Both Anti-A and Anti-B antibodies

  • Can donate blood to anyone (universal donor)

Blood Agglutination

• It happens when antibodies in the recipient’s plasma attack antigens on the donor’s red blood cells

• This immune reaction can block blood vessels and cause severe complications

Rh Factor

• a type of protein on the surface of red blood cells that can trigger an immune response if mismatched between donor and recipient

• If you have this antigen, you are Rh-positive.

• If you don’t have this antigen, you are Rh-negative.

• Type O Blood as a donor

  • Type O blood is considered a universal donor for red blood cells because it lacks A and B antigens, meaning it won’t trigger agglutination due to antigens

  • However, Type O plasma contains anti-A and anti-B antibodies, which can attack the recipient’s RBCs if these antibodies are not removed

• Can Type O Blood Be Transfused to Type B?

  • Red Blood Cells from Type O can safely be transfused to Type B because they don’t carry A or B antigens

  • Plasma from Type O, containing anti-B antibodies, may cause problems unless it is filtered or used in very small quantities

• Do Rh-positive or Rh-negative individuals have antibodies for Rh?

  • If you are Rh-positive, you do not have antibodies against Rh because your blood cells have the Rh antigen (positive marker).

  • If you are Rh-negative, your immune system can produce anti-Rh antibodies only if exposed to Rh-positive blood (e.g., through a blood transfusion or during pregnancy with an Rh-positive baby).

• Can an Rh-positive man and Rh-negative woman have a normal child?

  • Yes, it is possible to have a normal child, but there are risks depending on the Rh status of the baby:

    • There is no issue if the child is Rh-negative (inherited from the mother).

    • If the child is Rh-positive (inherited from the father), the mother’s immune system might produce anti-Rh antibodies. These antibodies can attack the baby’s red blood cells in subsequent pregnancies, leading to hemolytic disease of the fetus and newborn (HDFN).

• When and how does this happen physiologically?

  • During pregnancy or delivery, fetal Rh-positive blood cells can mix with the mother’s Rh-negative blood.

  • The mother’s immune system recognizes Rh-positive cells as foreign and produces anti-Rh antibodies (sensitization).

  • In subsequent pregnancies, if the fetus is Rh-positive, these antibodies can cross the placenta and attack the baby’s red blood cells, causing anemia, jaundice, or more severe complications.

• Hemolytic Disease of the Newborn

  • HDN happens when an Rh-negative mother is pregnant with an Rh-positive baby.

    • The mother’s immune system may produce antibodies against the Rh-positive blood cells of the baby, which can attack the baby’s red blood cells.

  • How to prevent it?

    • The solution is an injection called RhoGAM:

      • What is RhoGAM?

        • A medication that stops the mother’s immune system from producing antibodies against Rh-positive cells.

      • Why is it effective?

        • RhoGAM destroys Rh-positive fetal cells in the mother’s bloodstream before her immune system reacts to them.

Coagulation

• Refers to any clumping process

• Thrombosis in terms of blood

• Initiation

  • Extrinsic Pathway - Tissue Factor III (TFIII) from perivascular tissue

  • Intrinsitc Pathway - Exposure to endothelial collagen

Intrinsic Pathway for Coagulation

• Triggered when damage occurs inside the blood vessel, exposing collagen.

• Steps:

  • Factor XII is activated to XIIa.

  • Factor XI is activated to XIa.

  • Factor IX is activated to IXa, with help from calcium (Ca²⁺) and Factor VIIIa.

Extrinsic Pathway for Coagulation

• Triggered by damage to external tissues releasing tissue factor (Factor III).

• Steps:

  • Factor VII is activated to VIIa, combining with tissue factor to activate the common pathway.

Common Pathway for Coagulation

• Both intrinsic and extrinsic pathways lead here. The goal is to create fibrin, a protein that stabilizes the clot.

• Steps:

  • Factor X is activated to Xa, with help from Factor Va and calcium.

  • Prothrombin (Factor II) is converted to Thrombin (Factor IIa).

  • Thrombin activates Fibrinogen (Factor I) into Fibrin (Ia).

  • Fibrin forms a mesh to stabilize the clot, strengthened by Factor XIII.

Coagulation Disorders

• Hemophilia A - Factor VIII deficiency

• Hemophilia B - Factor IX deficiency

• Vitamin K Deficiency - affects factors II, VII, IX, X

Clotting Cascade

• Injury to the Vessel Wall

  • When a blood vessel is injured, collagen (a structural protein) is exposed in the vessel wall.

  • This triggers platelets to stick to the injured site and start forming a platelet plug.

• Platelet Activation

  • The platelets release chemical signals like:

    • Adenosine diphosphate (ADP): Helps recruit more platelets to the site.

    • Thromboxane A₂: Strengthens platelet aggregation (platelets sticking together).

• Clot Formation

  • More platelets stick together, and a network of fibrin forms to stabilize the plug, creating a clot that stops bleeding.

• Role of Prostacyclin and Nitric Oxide

  • These are chemicals released by healthy endothelial cells (cells lining the blood vessels) to:

    • Prevent platelets from sticking to healthy areas of the blood vessel.

    • Inhibit unnecessary platelet aggregation.

    • This ensures the clot is only formed at the injury site and not elsewhere.

Anti Clotting

• Endothelial Cells Release Anti-Clotting Substances:

  • Nitric Oxide (NO) and Prostacyclins: Keep blood vessels relaxed and prevent platelets from clumping together.

  • Protein C and Protein S:

    • Protein C inactivates clotting factors Va and VIIIa, stopping the clotting process.

    • Protein S helps Protein C by reducing thrombin (the enzyme that forms clots)

  • TFPI (Tissue Factor Pathway Inhibitor): Blocks the early steps of the clotting cascade triggered by tissue factor.

  • Antithrombin III (AT): Works with naturally occurring heparins in the body to block thrombin and other clotting factors.

  • Drugs:

    • Unfractionated Heparin: Boosts Antithrombin III’s ability to block thrombin and stop clot formation.

Clotting Times (CT)

• Different Substances Affect Clotting Time:

  • Sodium Oxalate makes blood clot slower than Sodium Citrate due to differences in how they interact with calcium.

  • Surfaces matter: Blood clots slower on cotton than on smooth glass or paraffin.

• Temperature and Clotting:

  • Warm blood clots faster than cold blood, but blood proteins degrade at very high temperatures (e.g., 60°C).

  • Cold reduces bleeding but not due to clotting time.

• Mixing Blood:

  • Mixed blood clots faster because of increased interaction between clotting factors.

• Spontaneous Clotting:

  • If natural anticoagulants (like Protein C or Antithrombin) are absent, blood can form clots even without an injury.

Blood pigments

• Proteins that bind oxygen and carry it through the bloodstream to supply tissues

• Conjugated Proteins - These pigments are combined with metal ions like iron (Fe²⁺) or copper (Cu²⁺) to help bind oxygen.

• Quickly and Reversibly Attaches Oxygen

  • Oxygen binding is reversible (e.g., oxygen attaches to hemoglobin when in the lungs and detaches in tissues).

  • This ensures oxygen delivery while maintaining a concentration gradient for efficient diffusion.

• Visual Effect:

  • Deoxygenated blood (no oxygen attached) appears darker.

  • Oxygenated blood (oxygen attached) appears bright red.

• Other Blood pigments in animals:

  • Hemoglobin - Fe²⁺ - Vertebrates (except Channichthyidae fish)

  • Hemocyanin - Cu²⁺ - Mollusks, arthropods, insects

  • Hemerythrin - Fe²⁺ - Marine invertebrates (e.g., sipunculids)

  • Chlorocruorin - Fe²⁺ - Marine worms

Phosphate Buffer

• Weak Acid - Sodium Dihydrogen Phosphate

• Weak Base - Sodium Monohydrogen Phosphate

• pK: 6.8

• Charged regionds of proteins can bind hydrogen and hydroxyl ions, and thus function as buffers

TOPIC: PROCESSES OF BREATHING IN HUMANS

Basic function of respiration

• Oxygen in:

  • Oxygen is taken into the body through the lungs and transported to cells for cellular metabolism (energy production).

  • It is also essential for maintaining blood pH, keeping it balanced.

• Carbon Dioxide out:

  • Carbon dioxide, a byproduct of metabolism, is removed from the body through exhalation.

  • If CO₂ accumulates, it becomes toxic and can disrupt pH balance.

• Muscles involved in respiration - External intercostals and diaphragm

Normal Breathing Pattern

• Inspiration - Diaphragm contracts, External intercostal muscles contract, and thoracic cavity expands

• Expiration - Thoracic cavity reduces and External intercostal muscles relax

• Chemoreceptors

  • Central Chemoreceptors (found in medulla):

    • Detect changes in CO₂ levels and pH in cerebrospinal fluid (CSF).

    • High CO₂ levels or low pH triggers faster breathing to remove excess CO₂.

  • Peripheral Chemoreceptors (in carotid and aortic bodies):

    • Sense oxygen (O₂) and carbon dioxide (CO₂) levels in the blood.

    • Low oxygen or high CO₂ signals the body to breathe faster or deeper.

• Pulmonary Strech Receptors

  • Found in the bronchi and bronchioles (airways in the lungs).

  • Prevent over-expansion of the lungs by triggering a reflex called the Hering-Breuer reflex:

    • This reflex signals the brain to stop inhalation when the lungs are full.

Dorsal Respiratory Group (DRG)

• Location: Medulla

• Function:

  • Acts as a pacemaker for normal breathing rhythm (quiet breathing).

  • Receives sensory input from vagus and glossopharyngeal nerve carrying input from:

    • Peripheral Chemoreceptors (monitor CO₂, O₂, and pH).

    • Baroreceptors (monitor blood pressure).

    • Stretch receptors (detect lung expansion).

  • Sends signals to control the diaphragm and external intercostal muscles, initiating inhalation.

Ventral Respiratory Group (VRG)

• Location: Medulla

• Function:

  • Becomes active during forced breathing (e.g., exercise).

  • Controls accessory respiratory muscles for deep inhalation and exhalation.

  • Contains the pre-Bötzinger complex (main generator of respiratory rhythm)

Pontine Respiratory Group (PRG)

• Location: Pons

• Function:

  • Coordinates smooth transitions between inhalation and exhalation.

  • Subdivided into two centers:

    • Pneumotaxic Center:

      • Limits inspiration duration by inhibiting the DRG.

    • Apneustic Center:

      • Prolongs inspiration by stimulating the DRG and VRG.

      • Works with the pneumotaxic center to maintain balance.

      • If damaged, it can cause apneustic breathing (long inhalation followed by short, ineffective exhalation).

Effect of Hyperventilation

• Rapid Breathing

  • Breathing too fast decreases carbon dioxide (CO₂) levels in the blood, a condition called hypocapnia.

  • CO₂ is crucial for maintaining proper pH levels in the blood. When CO₂ levels drop:

    • Blood becomes more alkaline (higher pH).

    • This also increases the pH of the cerebrospinal fluid (CSF) around the brain.

• Chemoreceptor Suppression

  • Central chemoreceptors in the brain (which monitor CO₂ and pH) reduce their activity because of the low CO₂ levels.

  • This can lead to temporary pauses in breathing, called apnea, as the body tries to reset its CO₂ balance.

• Subsequent Breathing

  • After hyperventilation, breathing becomes shallow or slows down as the body adjusts and CO₂ levels return to normal.

Effect of Hyperventilation in Closed System

• Rebreathing CO₂:

  • When you hyperventilate in a closed system, you breathe in the CO₂ you previously exhaled.

  • This prevents blood CO₂ levels from dropping too low (avoids hypocapnia, which happens in open-air hyperventilation).

• Effects on Breathing:

  • Rebreathing CO₂ helps maintain normal blood CO₂ levels and reduces the risk of apnea (temporary cessation of breathing).

  • The hyperventilation period is shorter because CO₂ levels stay balanced, so the body doesn’t need to adjust as dramatically.

Effect of Rebreathing Expired Air

• CO₂ Levels Increase:

  • Since exhaled air contains carbon dioxide (CO₂), rebreathing it leads to an accumulation of CO₂ in your blood. This is called hypercapnia.

  • High CO₂ levels stimulate the central and peripheral chemoreceptors, which monitor CO₂ and pH levels.

• Body’s Response:

  • The body reacts by increasing the rate and depth of breathing to expel the excess CO₂ and maintain a stable blood pH.

• Benefits in a Closed System:

  • Rebreathing reduces the likelihood and severity of apnea (pauses in breathing) compared to hyperventilating in open air, as CO₂ levels remain higher and stable.

Effects of Pain Stimuli

• Before Pain (Normal Breathing)

  • Breathing is steady and rhythmic under calm conditions.

  • Controlled by the balance of oxygen (O₂) and carbon dioxide (CO₂) levels in the body.

• During Pain

  • Stress or Anxiety:

    • Triggers the sympathetic nervous system, causing shallow and rapid breathing (hyperventilation).

  • Pain:

    • Can disrupt normal breathing, leading to irregular patterns or short pauses (apnea) due to the discomfort or reflexive reactions.

• After Pain (Relaxation)

  • Relaxation or Positive Emotions:

    • Activates the parasympathetic nervous system, which slows and deepens breathing.

    • Breathing becomes more regular as the body recovers and returns to its normal state.

Effect of Mental Concentration

• Influence of the Brain:

  • Higher brain centers, like the central cortex, modulate breathing when you are focusing.

  • These brain signals influence the medullary respiratory center (the part of the brainstem that controls breathing).

• Breathing Changes:

  • Focused state:

    • Breathing usually becomes slower and shallower as you concentrate deeply.

  • Stress during concentration:

    • If stress is involved, breathing may become faster and deeper.

Sympathetic Autonomic Nervous System (SANS) vs Parasympathetic Autonomic Nervous System (PANS)

• Sympathetic Nervous System (SNS):

  • What It Does:

    • Causes bronchodilation (airways widen).

  • How It Works:

    • Releases norepinephrine and epinephrine (stress hormones).

    • These hormones bind to beta-2 adrenergic receptors in the smooth muscles of the airways.

    • This relaxes the muscles, making it easier to breathe.

• Parasympathetic Nervous System (PNS):

  • What It Does:

    • Causes bronchoconstriction (airways narrow) and increases mucus secretion.

  • How It Works:

    • Releases acetylcholine (a neurotransmitter) through the vagus nerve.

    • Acetylcholine activates muscarinic (M3) receptors in the smooth muscles of the airways.

    • This makes the muscles contract, narrowing the airways.

Effect of Breath Holding

• Trigger Reflex:

  • Breath-holding stimulates a reflex that:

  • Lowers heart rate.

  • Causes vasoconstriction (narrowing blood vessels) to preserve oxygen for vital organs.

• Increasing CO₂ & Decreasing O₂:

  • CO₂ buildup triggers the urge to breathe.

  • Lower oxygen can cause discomfort or fainting.

• Hyperventilation - Reduces initial CO₂ levels, delaying the urge to breathe but increasing the risk of hypoxic blackout (fainting due to low oxygen).

• Maximal forced expiration - Leaves little oxygen in the lungs, making it harder to hold your breath (elevated CO2 levels)

Effect of Drinking

• Swallowing and the Airway:

  • The act of swallowing is coordinated by central pattern generators in the brainstem.

  • To prevent choking, the epiglottis (a flap in the throat) closes over the airway, temporarily blocking airflow.

• Respiratory Pause (Swallow Apnea):

  • While swallowing, there is a brief pause in breathing known as swallow apnea.

  • This pattern follows a sequence:

    • Exhalation → Pause → Exhalation resumes.

    • The pause ensures that liquids or food do not enter the airway.

Effect of Speech

• Inspiration (Inhalation):

  • The time spent inhaling becomes shorter, and the speed of inhalation increases to quickly bring in air needed for speaking.

  • This ensures there is enough air in the lungs to support vocalization.

• Expiration (Exhalation):

  • The time spent exhaling becomes longer to allow for controlled release of air while producing sounds.

  • The speed of exhalation slows down to provide steady airflow for speaking and forming words.

Effect of Obstruction of Respiratory Passageways

• Increased Airway Resistance:

  • The obstruction makes it harder for air to flow in and out of the lungs, increasing the effort needed to breathe.

• Breathing Changes:

  • Breaths become slower but deeper as the body tries to compensate for the reduced airflow by taking in more air with each breath.

• Examples of Conditions:

  • Asthma: Narrowing of airways due to inflammation.

  • Chronic Obstructive Pulmonary Disease (COPD): Long-term airway narrowing or damage.

  • Obstructive Sleep Apnea: Temporary airway blockage during sleep.

Effect of Laughing/Coughing

• Coughing:

  • What Happens:

    • Coughing is a forceful expiration (blowing air out).

    • It temporarily interrupts normal breathing patterns to clear the airways.

  • Respiratory Changes:

    • Increases the amplitude (size) of respiratory movements due to the strong force of exhalation.

• Laughing:

  • What Happens:

    • Laughing involves rhythmic contractions of the respiratory muscles.

  • Respiratory Changes:

    • Rapid, shallow breaths occur during laughing episodes.

    • Followed by deeper inhalations to bring in more air after the laughter.

Effect of Exercise

• What Happens During Exercise?

  • Increased Metabolic Demands:

    • Your body needs more oxygen (O₂) for energy.

    • It also produces more carbon dioxide (CO₂) as a waste product, which must be removed.

  • Respiratory Changes:

    • The respiratory centers in the medulla (part of the brainstem) signal faster and deeper breathing (ventilation) to meet the body’s needs.

  • Chemoreceptor Activity:

    • Central and peripheral chemoreceptors (in the brain, carotid arteries, and aorta) detect:

      • Rising CO₂ levels.

      • Decreasing blood pH (becomes more acidic due to CO₂ buildup).

    • These signals trigger increased breathing to restore balance.

• What Happens During Intense or Prolonged Exercise?

  • Hyperthermia:

    • The body overheats, further increasing the demand for oxygen and the rate of ventilation.

  • Anaerobic Metabolism:

    • If oxygen supply cannot keep up, cells switch to anaerobic metabolism, producing lactic acid and further lowering blood pH.

  • Sympathetic Nervous System:

    • This system (activated during stress and exercise) increases ventilation to deliver more oxygen to the muscles.

TOPIC: MICROCIRCULATION

Leukocytes

• White blood cells

• Phagocytic (engolf and digest particles)

• First level of protection against foreign parasites

• Produced by the bone marrow

• Distributed along blood and lymph tissue

• Different types:

  • Neutrophils:

    • Kill bacteria, fungi, and foreign debris.

    • Are the most abundant type of leukocytes and are involved in fighting infections.

  • Monocytes:

    • Clean up damaged cells and debris.

    • They can differentiate into macrophages when they move into tissues and play a role in phagocytosis.

  • Eosinophils:

    • Kill parasites and cancer cells.

    • Involved in allergic responses and inflammation.

  • Lymphocytes:

    • Help fight viruses and make antibodies.

    • Include T cells, B cells, and natural killer (NK) cells, all of which are essential for adaptive immunity.

  • Basophils:

    • Play a role in allergic responses.

    • Release histamine and other chemicals to mediate inflammation.

Microcirculation

• The flow of blood through the smallest blood vessels in the circulatory system

• Maintains homeostasis (through the transport of oxygen and other substances to tissue cells)

• Transports CO2, lactic acid, nitrogenous products from tissue cells to environment

Vasomotion

• Rhythmic spontaneous oscullation of smooth muscle that surrounds blood vessels

• Regulate blood pressure

• Optimize tissue perfusion (ensures tissues receive adequate amounts of oxygen)

• Two types:

  • Vasoconstriction

    • Prolonged contraction of smooth muscles surrounding blood vessels

    • Decrease in blood vessel diameter

    • Increase in blood flow rate

    • Vasoconstrictors in the experiment:

      • Nicotine

      • Adrenaline Chloride

      • Pain

      • Cold Ringer’s

  • Vasodilation

    • Relaxation of smooth muscles surrounding blood vessels

    • Increase in blood vessel diameter

    • Decrease in blood flow rate

    • Vasodilators in the experiment:

      • Lactic Acid

      • Histamine Acid Phosphate

      • Acetylcholine Bromide

      • Absolute Ethanol

      • Sodium Bromide

      • Warm Ringer’s

Blood Vessels in the Webbed Feet of the Frog

• Arteriole

  • Blood Vessel Diameter: Thickest

  • Blood Flow: Fastest

• Venule

  • Blood Vessel Diameter: Thicker than capillary; thinner than arteriole

  • Blood Flow: Faster than capillary; slower than arteriole

• Capillary

  • Blood Vessel Diameter: Thin

  • Blood Flow: Slower

Effect of stimuli on blood vessel diameter and flow rate

Group A:

• Lactic Acid

  • Blood Vessel Diameter - increase

  • Blood Flow Rate - decrease

• Histamine Acid Phosphate

  • Blood Vessel Diameter - increase

  • Blood Flow Rate - decrease

• Acetylcholine bromide

  • Blood Vessel Diameter - increase

  • Blood Flow Rate - decrease

• Absolute Ethanol

  • Blood Vessel Diameter - increase

  • Blood Flow Rate - decrease

• Sodium Bromide

  • Blood Vessel Diameter - increase

  • Blood Flow Rate - decrease

• Warm Ringer’s

  • Blood Vessel Diameter - increase

  • Blood Flow Rate - decrease

Group B:

• Nicotine

  • Blood Vessel Diameter - decrease

  • Blood Flow Rate - increase

• Adrenaline Chloride

  • Blood Vessel Diameter - increase

  • Blood Flow Rate - decrease

• Pain

  • Blood Vessel Diameter - decrease

  • Blood Flow Rate - increase

• Cold Ringer’s

  • Blood Vessel Diameter - decrease

  • Blood Flow Rate - increase

Blood Vessels

• Artery

  • Highest velocity

  • Smallest cross-sectional area

  • Pulsatile flow (pulsating movement of blood)

• Capillary

  • Lowest velocity

  • Largest cross sectional area

  • Pulsatile

• Vein

  • Velocity higher than capillaries but lower than arteries

  • Smooth flow

Pathways that control the diameter of blood vessels

• Cholinergic Pathway

  • Secretes Nitric Oxide (NO) as a smooth muscle relaxant

    • Increases blood flow by reducing resistance in the vessel.

  • Causes Vasodilation

• Noradrenergic Pathway

  • Causes Vasoconstriction, which can lead to increased blood pressure and reduced blood flow to certain areas.

Response to temperature

• Receptors in skin

  • Thermo-sensitive receptors detect temperature changes.

  • There are more cold receptors than warm ones.

  • These receptors send signals to the brain to adjust the body’s responses.

• Body’s response to hot temperature:

  • Sympathetic Inhibition:

    • The posterior hypothalamus, which controls blood vessel tone, is inhibited in hot conditions.

    • This reduces signals that would constrict blood vessels.

  • Vasodilation:

    • Cholinergic neurons release acetylcholine, which causes blood vessels to relax and widen (vasodilation).

    • This increases blood flow to the skin to release heat.

  • Effects on the Body:

    • Increased blood flow rate: Helps transfer heat to the skin for cooling.

    • Decreased blood pressure: Due to the widened blood vessels.

  • Body’s response to cold temperature:

    • Sympathetic Centers Are Activated:

      • The posterior hypothalamus (a brain area that controls body temperature) activates the sympathetic nervous system.

    • Vasoconstriction:

      • This activation causes blood vessels to narrow (vasoconstriction), reducing blood flow to the skin and extremities to conserve heat.

    • Role of Norepinephrine:

      • The body releases norepinephrine (a chemical messenger).

      • Norepinephrine binds to adrenergic receptors on blood vessel walls, causing smooth muscles to contract, which leads to the narrowing of the vessels.

Acetylcholine and Nitric Oxide for Vasodilation

• Acetylcholine Binds to Receptors:

  • Acetylcholine attaches to a specific receptor called the muscarinic 3 acetylcholine receptor on endothelial cells (cells lining blood vessels).

  • This activates the production of nitric oxide (NO) inside the endothelial cells.

• Nitric Oxide is Released:

  • Nitric oxide acts as a relaxing factor for blood vessels.

  • It diffuses into nearby smooth muscle cells in the blood vessel wall.

• Muscle Relaxation:

  • Inside the smooth muscle cells, nitric oxide reduces calcium ion levels, which relaxes the muscle and causes the blood vessel to widen (vasodilation).

• Role of L-Arginine and cGMP

  • L-Arginine:

    • Nitric oxide is made from L-arginine with the help of an enzyme called endothelial nitric oxide synthase.

  • cGMP (Cyclic Guanosine Monophosphate):

    • Nitric oxide activates guanylyl cyclase, which produces cGMP.

    • cGMP reduces signals for blood vessel constriction and relaxes the smooth muscle further.

• Summary:

  • Increased Blood Flow:

    • Vasodilation improves blood flow to tissues.

  • Reduced Blood Pressure:

    • Widened blood vessels decrease resistance, lowering blood pressure.

  • Controlled Sympathetic Activity:

    • cGMP also helps prevent excessive constriction of blood vessels.

Norepenephrine causing vasocontriction

• At Low Doses:

  • Norepinephrine activates beta-1 adrenergic receptors, which can cause vasodilation (widening of blood vessels).

• At Higher Doses:

  • It activates alpha-1 and alpha-2 adrenergic receptors, which cause vasoconstriction (narrowing blood vessels).

• Alpha-1 Receptor Activation:

  • When norepinephrine binds to alpha-1 receptors:

    • It triggers a series of reactions inside the smooth muscle cells of blood vessels.

    • This increases the calcium ion levels in the cells.

    • Calcium ions are essential for muscle contraction, which causes the blood vessels to constrict.

• Alpha-2 Receptor Activation:

  • Norepinephrine binds to alpha-2 receptors on smooth muscle cells.

  • This reduces the activity of adenylate cyclase, an enzyme responsible for producing cAMP (a signaling molecule).

  • Lower cAMP levels lead to contraction of the smooth muscle, causing the blood vessel to narrow.

• Phospholipase C Activation:

  • Norepinephrine also activates phospholipase C, another enzyme in the smooth muscle cell.

  • This enzyme helps increase calcium ions inside the cell.

  • Higher calcium levels make the smooth muscle contract, further contributing to vasoconstriction.

• Key effects:

  • Vasoconstriction:

    • Narrowing blood vessels increases systemic vascular resistance (the effort required to pump blood), which can raise blood pressure.

  • Increased Calcium Ions:

    • The rise in extracellular calcium ions strengthens the contraction of the smooth muscle in the blood vessel walls.

  • Norepinephrine triggers a series of reactions inside blood vessel muscles to tighten them, reducing the size of the vessel and increasing blood pressure.

Adrenoreceptors

• Adrenoreceptors are G protein-coupled receptors targeted by chemicals like norepinephrine and epinephrine.

• They belong to the sympathetic nervous system, which controls the “fight or flight” response.

• Two main types:

  • Alpha receptors (α): Focus on constricting blood vessels (vasoconstriction) and increasing blood pressure.

  • Beta receptors (β): Focus on relaxing muscles (vasodilation) and increasing heart activity.

• Catecholamine Dependence

  • Effects depend on the level of norepinephrine or epinephrine:

    • High levels: Alpha activation (vasoconstriction).

    • Low levels: Beta activation (vasodilation).

• Alpha vs Beta Adrenergic Receptors:

  • Beta Receptor Activation:

    • Activates adenylate cyclase, increasing cAMP (a signaling molecule).

    • cAMP effects:

      • Relaxes smooth muscles (vasodilation).

      • Increases heart contraction and cardiac output.

      • Promotes heart muscle activity, smooth muscle relaxation, and reduces blood vessel resistance.

  • Alpha Receptor Activation:

    • Reduces cAMP levels:

      • This increases smooth muscle contraction, leading to vasoconstriction.

    • Alpha-1 receptors:

      • Increase calcium ions, strengthening blood vessel contraction.

    • Alpha-2 receptors:

      • Lower cAMP, reinforcing vasoconstriction.

      • Alpha receptors are less sensitive than beta receptors, requiring higher norepinephrine levels.

  • Key Takeaways:

    • Alpha receptors:

      • Cause vasoconstriction (narrowing blood vessels).

      • Raise blood pressure and redirect blood flow to vital organs.

    • Beta receptors:

      • Cause vasodilation (widening blood vessels).

      • Increase blood flow and improve heart performance.

Vasocontrictors:

• Nicotine

  • Nicotine activates the sympathetic nervous system, which is responsible for “fight or flight” responses.

  • Release of norepinephrine:

    • Nicotine causes the release of norepinephrine, a chemical that binds to alpha-1 adrenergic receptors on blood vessels.

    • This binding activates enzymes that lead to vasoconstriction (narrowing of blood vessels).

  • Nicotine’s action on receptors:

    • Initially, nicotine binds to nicotinic receptors, triggering the release of sodium and calcium ions.

    • These ions create an electrical signal (depolarization) that further stimulates the release of norepinephrine.

  • Low cAMP levels:

    • The process reduces cAMP (cyclic adenosine monophosphate) levels, promoting muscle contraction in blood vessel walls, further enhancing vasoconstriction.

• Adrenaline

  • Activates the Sympathetic Nervous System:

    • Adrenaline stimulates your “fight or flight” system, preparing your body to respond to stress.

  • Alpha-1 Receptors:

    • Adrenaline binds to alpha-1 receptors in blood vessels, causing smooth muscles in the vessel walls to contract. This leads to vasoconstriction, which increases blood pressure.

    • Higher doses of adrenaline are required to activate these receptors.

  • Beta Receptors:

    • Adrenaline also acts on beta receptors, which can cause effects like vasodilation (relaxation of vessels) at lower doses and increased heart rate.

  • cAMP and Calcium:

    • Adrenaline regulates cAMP (cyclic adenosine monophosphate) and calcium ion levels in cells:

      • Alpha-1: Causes an increase in calcium, leading to contraction.

      • Beta: Increases cAMP, leading to relaxation in smooth muscles and stronger heart contractions

• Pain/Stress

  • Stress Response:

    • Pain triggers a stress response, activating the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system, which prepares the body to handle stress or injury.

  • Release of Hormones:

    • Cortisol and catecholamines (like adrenaline and norepinephrine) are released. These hormones increase blood pressure by causing vasoconstriction (narrowing of blood vessels).

  • Noxious Stimuli:

    • Painful (noxious) signals can cause different effects on blood vessels in the skin (cutaneous) and muscles. For example:

      • Cutaneous vessels: Tighten to reduce blood flow.

      • Muscle vessels: May adjust differently based on the pain signal.

Vasodilators:

• Histamine and Phosphate

  • Histamine Receptors:

    • Histamine binds to Histamine-2 Receptors (H2R) in neurons and adrenal glands, triggering vasodilation (widening of blood vessels).

    • It can also bind to H1, H3, and H4 receptors, but its effects depend on the specific receptor and location (some may cause vasoconstriction instead).

  • Production of Vasodilators:

    • The signaling process activates enzymes that produce prostacyclin and nitric oxide. These chemicals relax the smooth muscles in blood vessel walls, allowing the vessels to widen.

• Acetylcholine Bromide

  • Binds to muscarinic 3 acetylcholine receptor regulating nitric oxide release

• Absolute Ethanol

  • Increases nitric oxide production through stimulation of nitric oxide synthase

• Lactic Acid

  • Lactic Acid from Exercise:

    • When muscles work hard, they produce lactic acid as a result of increased glycolysis (breaking down glucose for energy).

    • Lactic acid can lower the pH (make it more acidic), which helps relax blood vessels and increase blood flow.

  • Anaphylactic Shock:

    • In extreme cases, lactic acid and inflammatory responses (like from anaphylactic shock) release histamine, which widens blood vessels (vasodilation).

    • This can lead to a drop in blood pressure.

  • Inflammation:

    • Inflammation causes blood vessels to widen further, promoting blood flow to affected areas.

  • Potassium Ions:

    • Muscles release potassium ions during activity, which also helps relax blood vessels by lowering the pH.

  • Nitric Oxide:

    • All these conditions stimulate the release of nitric oxide, a chemical that relaxes smooth muscles in blood vessel walls, allowing for vasodilation.

• Sodium Bromide

  • Regulating Blood pH:

    • The blood’s pH is controlled by systems like the sodium-hydrogen exchanger and the bicarbonate-chloride antiporter. These systems help maintain the acid-base balance.

  • Effect of Excess Sodium:

    • Too much sodium can change the blood’s pH. This affects how well the heart and blood vessels respond to molecules like:

      • Angiotensin II

      • Endothelin-1

      • Alpha-adrenergic agonists

      • These molecules normally cause vasoconstriction (narrowing of blood vessels).

  • Reduced Inotropic Response:

    • Sodium bromide reduces the strength of these molecules’ effects, leading to less blood vessel constriction.

Starling Forces

• Physical forces responsible for the determination of fluid movement between the tissues and capillaries

• Types of Starling Forces

  • Hydrostatic Pressure

    • Pressure that any fluid in a confined space exerts

  • Oncotic Pressure

    • Pressure created by colloids in a fluid preventing the movement of water from one solution across a semipermeable membrane into another solution or vice versa