Blood Flow and the Control of Blood Pressure

Blood Flow and Blood Pressure Control

Factors Controlling Blood Vessel Resistance

• Local Control Systems: These systems regulate the size of blood vessels.

• Sympathetic Reflexes: Cardiac reflexes are essential for controlling blood vessel size.

• Hormones: Hormones can influence blood vessel size.

Vasoconstriction and Vasodilation Factors

• Vasoconstrictors:

  • Vasopressin

  • Angiotensin II: Target of ACE inhibitors.

  • Serotonin

  • Norepinephrine: Acts on alpha receptors.

• Vasodilators:

  • Epinephrine: Acts via beta-2 receptors.

  • Acetylcholine: Dilates blood vessels in muscles during contraction.

  • Nitric Oxide: Released from endothelium.

  • Bradykinin

  • Adenosine

  • Low Oxygen Levels: Signals need for more blood.

  • High Carbon Dioxide Levels: Signals need for more blood.

  • High Acid Levels (Hydrogen ions): Signals need for more blood.

  • High Potassium Levels: Signals need for more blood.

  • Histamine: Vasodilator during allergic reactions.

  • Natriuretic Peptides

Natriuretic Peptides

• Triggered by high blood pressure causing stretch in the atria of the heart and brain tissue.

• Cause the kidneys to release sodium into the urine (natriuresis).

• Water follows sodium, reducing blood volume and blood pressure. Blood pressure P depends on volume V.

• Types:

  • Atrial Natriuretic Peptide (ANP): Comes from the atria of the heart.

  • Brain Natriuretic Peptide (BNP): Comes from the brain.

Arteriolar Resistance Control Mechanisms

• Myogenic Autoregulation: Regulation by smooth muscles themselves; involves calcium.

• Paracrine: Activated by hyperemia (excess blood flow) and adenosine.

• Neural and Hormonal Signals: Primarily from the endocrine system.

  • Sympathetic control via cardiac reflexes.

  • Effects of norepinephrine and epinephrine (from adrenal medulla).

Hyperemia

• Active Hyperemia: Increased blood supply due to metabolic activity (e.g., during muscle use).

• Reactive Hyperemia: Increased blood flow after a temporary obstruction is removed (e.g., after releasing a tourniquet). Follows removal of a clot or embolism.

Sympathetic and Parasympathetic Effects on Blood Vessels

• Parasympathetic nervous system does not have a direct effect on blood vessels.

• Blood vessels have smooth muscle attached to sympathetic neurons.

• Mechanism:

  • Sympathetic innervation controls blood vessel tone.

  • Normal tone: Maintained by a baseline level of sympathetic activity (e.g., dial switch at 5).

  • Vasoconstriction: Increased sympathetic activity (dial up to 10).

  • Vasodilation: Reduced sympathetic activity (dial down to 0); parasympathetic reduces sympathetic innervation.

Cardiovascular Control Center

• Located in the medulla oblongata.

• Receives input from baroreceptors (baroreceptor reflexes).

Baroreceptor Reflex Arc

1. Receptors: Baroreceptors in the aorta and carotid artery detect blood pressure changes.

2. Sensory Neurons: Relay information to the cardiovascular control center.

3. Control Center: Medulla oblongata (medullary cardiovascular control center).

4. Motor Neurons: Autonomic nervous system (sympathetic and parasympathetic).

   • Parasympathetic: Slows down the heart, leading to indirect relaxation of blood vessels and lower blood pressure.

   • Sympathetic: Speeds up the heart (sinoatrial node), increases ventricular contraction, constricts arterioles, and increases blood pressure.

5. Effectors: Heart muscle and smooth muscle of blood vessels.

Response to High Blood Pressure

• Baroreceptors in the aorta and carotid artery detect distension.

• Medulla oblongata increases parasympathetic activity and decreases sympathetic activity.

• Effects:

  • Vasodilation: Reduces peripheral resistance, lowering blood pressure.

  • Slowing of Heart Rate: Parasympathetic activity reduces heart rate (SA node), decreasing cardiac output and blood pressure.

Capillary Exchange

• Exchange occurs across thin capillary walls (simple squamous epithelium) and venules.

• Capillary density is related to tissue metabolic activity.

• Types of Capillaries:

  • Continuous Capillaries: Leaky junctions.

  • Fenestrated Capillaries: Large pores, more permeable to larger molecules like plasma proteins.

Bulk Flow

• Filtration: Movement of fluid from capillaries to the outside, driven by hydrostatic pressure at the arterial end.

• Absorption: Movement of fluid into the capillaries, driven by colloid osmotic pressure at the venous end.

Lymphatic System Functions

• Returns fluid and proteins to the circulatory system.

• Picks up and transfers absorbed fats into the circulatory system from the GI tract.

• Filters pathogens.

Fluid Movement

• Fluid moves from capillaries to interstitial compartment to cells and back.

• Outward Movement: Hydrostatic pressure (blood pressure) pushes fluid out of capillaries.

• Inward Movement: Plasma proteins (e.g., albumin) generate osmotic, oncotic, or colloid pressure, drawing fluid back into capillaries.

Lymphatic Vessels

• Blind-ended vessels with one-way valves.

• Ensure fluid flow to the cardiovascular system.

• Larger holes than capillaries to accommodate escaping plasma proteins.

• Lymph Nodes: Checkpoints with T cells and B cells for surveillance.

  • Large lymph nodes indicate a problem (infection).

Summary of Lymphatic System

• Takes excess fluid from tissues back to cardiovascular system.

• Returns escaped plasma proteins to cardiovascular system.

• Surveillance for infection at lymph nodes.

Lymph Node Distribution

• Cervical Lymph Nodes: Drain oral cavity, ears, nose, and eyes.

• Axillary Lymph Nodes: Drain breast, chest, and upper body.

• Inguinal Lymph Nodes: Drain lower extremities.

Edema

• Excess fluid in the interstitial compartment.

• Causes:

  • Increased hydrostatic pressure.

  • Decreased plasma protein concentration.

  • Increased interstitial proteins.

  • Blockage of lymphatic drainage.

Cardiovascular Diseases

• Risk Factors:

  • Controllable: Smoking, overweight/obesity, lack of exercise, untreated hypertension.

  • Non-Controllable: Sex, age, family history.

Cholesterol

• High-Density Lipoprotein (HDL): "Good" cholesterol; empty vehicles for picking up trash (triglycerides).

• Low-Density Lipoprotein (LDL): "Bad" cholesterol; vehicles loaded with fat.

• Goal: High HDL and low LDL.

Atherosclerosis

• Inflammatory condition due to triglyceride buildup.

• Macrophages attempt to remove fat, injuring endothelium and exposing collagen.

• Platelets form a clot on top.

• Macrophages get trapped, enlarging the clot and obstructing blood flow.

• Unstable clots can dislodge and travel to the heart, lungs, or brain.

Hypertension

• High blood pressure.

• Risk of cardiovascular disease doubles with each 20/10 mmHg increase in blood pressure.

• Types:

  • Essential Hypertension: No clear cause (90% of cases); normal cardiac output but increased peripheral resistance.

  • Secondary Hypertension: Has an identifiable cause that can be fixed.

Factors Controlling Blood Vessel Resistance

• Local Control Systems: These systems regulate the size of blood vessels through mechanisms like autoregulation and paracrine signaling.

• Sympathetic Reflexes: Cardiac reflexes, mediated by the sympathetic nervous system, are crucial for controlling blood vessel size and overall blood pressure.

• Hormones: Various hormones, such as epinephrine and angiotensin II, can significantly influence blood vessel size and systemic vascular resistance.

Vasoconstriction and Vasodilation Factors

• Vasoconstrictors:

  • Vasopressin: Potent vasoconstrictor that also regulates water balance.

  • Angiotensin II: Target of ACE inhibitors; plays a key role in the renin-angiotensin-aldosterone system (RAAS) to increase blood pressure.

  • Serotonin: Primarily involved in platelet aggregation but also acts as a vasoconstrictor.

  • Norepinephrine: Acts on alpha receptors in blood vessels, causing constriction.

• Vasodilators:

  • Epinephrine: Acts via beta-2 receptors, causing vasodilation in muscle tissue.

  • Acetylcholine: Dilates blood vessels in muscles during contraction, enhancing blood flow to active muscles.

  • Nitric Oxide: Released from endothelium; a powerful vasodilator that plays a critical role in maintaining vascular tone.

  • Bradykinin: A peptide that causes vasodilation and increases vascular permeability.

  • Adenosine: Released during metabolic activity, causing vasodilation to increase blood flow to active tissues.

  • Low Oxygen Levels: Signals need for more blood, leading to vasodilation in hypoxic tissues.

  • High Carbon Dioxide Levels: Signals need for more blood, causing vasodilation to remove excess CO_2.

  • High Acid Levels (Hydrogen ions): Signals need for more blood; vasodilation helps remove excess acid.

  • High Potassium Levels: Signals need for more blood; vasodilation helps maintain ion balance.

  • Histamine: Vasodilator during allergic reactions, increasing blood flow and vascular permeability.

  • Natriuretic Peptides: Counteract the effects of angiotensin II and promote vasodilation.

Natriuretic Peptides

• Triggered by high blood pressure, causing stretch in the atria of the heart and brain tissue.

• Cause the kidneys to release sodium into the urine (natriuresis).

• Water follows sodium, reducing blood volume and blood pressure. Blood pressure P depends on volume V, according to the relationship P \propto V.

• Types:

  • Atrial Natriuretic Peptide (ANP): Comes from the atria of the heart, released in response to atrial stretch.

  • Brain Natriuretic Peptide (BNP): Comes from the brain and ventricles of the heart; used as a marker for heart failure.

Arteriolar Resistance Control Mechanisms

• Myogenic Autoregulation: Regulation by smooth muscles themselves; involves calcium-dependent mechanisms that respond to changes in blood pressure.

• Paracrine: Activated by hyperemia (excess blood flow) and adenosine, leading to vasodilation and increased blood supply.

• Neural and Hormonal Signals: Primarily from the endocrine system.

  • Sympathetic control via cardiac reflexes.

  • Effects of norepinephrine and epinephrine (from adrenal medulla).

Hyperemia

• Active Hyperemia: Increased blood supply due to metabolic activity (e.g., during muscle use), resulting from local vasodilation.

• Reactive Hyperemia: Increased blood flow after a temporary obstruction is removed (e.g., after releasing a tourniquet). Follows removal of a clot or embolism, allowing for rapid restoration of blood flow.

Sympathetic and Parasympathetic Effects on Blood Vessels

• Parasympathetic nervous system does not have a direct effect on most blood vessels (except in specific regions like the salivary glands).

• Blood vessels have smooth muscle attached to sympathetic neurons.

• Mechanism:

  • Sympathetic innervation controls blood vessel tone.

  • Normal tone: Maintained by a baseline level of sympathetic activity (e.g., dial switch at 5).

  • Vasoconstriction: Increased sympathetic activity (dial up to 10), leading to decreased blood flow.

  • Vasodilation: Reduced sympathetic activity (dial down to 0); parasympathetic reduces sympathetic innervation, indirectly causing vasodilation.

Cardiovascular Control Center

• Located in the medulla oblongata.

• Receives input from baroreceptors (baroreceptor reflexes) and chemoreceptors (detecting changes in blood pH and gas levels).

Baroreceptor Reflex Arc

1. Receptors: Baroreceptors in the aorta and carotid artery detect blood pressure changes.

2. Sensory Neurons: Relay information to the cardiovascular control center via the vagus and glossopharyngeal nerves.

3. Control Center: Medulla oblongata (medullary cardiovascular control center).

4. Motor Neurons: Autonomic nervous system (sympathetic and parasympathetic).

   • Parasympathetic: Slows down the heart, leading to indirect relaxation of blood vessels and lower blood pressure.

   • Sympathetic: Speeds up the heart (sinoatrial node), increases ventricular contraction, constricts arterioles, and increases blood pressure.

5. Effectors: Heart muscle and smooth muscle of blood vessels.

Response to High Blood Pressure

• Baroreceptors in the aorta and carotid artery detect distension.

• Medulla oblongata increases parasympathetic activity and decreases sympathetic activity.

• Effects:

  • Vasodilation: Reduces peripheral resistance, lowering blood pressure.

  • Slowing of Heart Rate: Parasympathetic activity reduces heart rate (SA node), decreasing cardiac output and blood pressure.

Capillary Exchange

• Exchange occurs across thin capillary walls (simple squamous epithelium) and venules.

• Capillary density is related to tissue metabolic activity; highly active tissues have more capillaries.

• Types of Capillaries:

  • Continuous Capillaries: Leaky junctions allowing for exchange of small molecules.

  • Fenestrated Capillaries: Large pores, more permeable to larger molecules like plasma proteins; found in kidneys and intestines.

Bulk Flow

• Filtration: Movement of fluid from capillaries to the outside, driven by hydrostatic pressure at the arterial end.

• Absorption: Movement of fluid into the capillaries, driven by colloid osmotic pressure at the venous end.

Lymphatic System Functions

• Returns fluid and proteins to the circulatory system.

• Picks up and transfers absorbed fats into the circulatory system from the GI tract.

• Filters pathogens via lymph nodes.

Fluid Movement

• Fluid moves from capillaries to interstitial compartment to cells and back.

• Outward Movement: Hydrostatic pressure (blood pressure) pushes fluid out of capillaries.

• Inward Movement: Plasma proteins (e.g., albumin) generate osmotic, oncotic, or colloid pressure, drawing fluid back into capillaries.

Lymphatic Vessels

• Blind-ended vessels with one-way valves.

• Ensure fluid flow to the cardiovascular system.

• Larger holes than capillaries to accommodate escaping plasma proteins.

• Lymph Nodes: Checkpoints with T cells and B cells for surveillance.

  • Large lymph nodes indicate a problem (infection).

Summary of Lymphatic System

• Takes excess fluid from tissues back to cardiovascular system.

• Returns escaped plasma proteins to cardiovascular system.

• Surveillance for infection at lymph nodes.

Lymph Node Distribution

• Cervical Lymph Nodes: Drain oral cavity, ears, nose, and eyes.

• Axillary Lymph Nodes: Drain breast, chest, and upper body.

• Inguinal Lymph Nodes: Drain lower extremities.

Edema

• Excess fluid in the interstitial compartment.

• Causes:

  • Increased hydrostatic pressure (e.g., due to heart failure).

  • Decreased plasma protein concentration (e.g., due to liver or kidney disease).

  • Increased interstitial proteins (e.g., due to inflammation).

  • Blockage of lymphatic drainage (e.g., due to surgery or infection).

Cardiovascular Diseases

• Risk Factors:

  • Controllable: Smoking, overweight/obesity, lack of exercise, untreated hypertension, high cholesterol, diabetes.

  • Non-Controllable: Sex, age, family history, genetic predisposition.

Cholesterol

• High-Density Lipoprotein (HDL): "Good" cholesterol; empty vehicles for picking up trash (triglycerides).

• Low-Density Lipoprotein (LDL): "Bad" cholesterol; vehicles loaded with fat; contributes to plaque formation in arteries.

• Goal: High HDL and low LDL to reduce risk of atherosclerosis.

Atherosclerosis

• Inflammatory condition due to triglyceride buildup in arterial walls.

• Macrophages attempt to remove fat, injuring endothelium and exposing collagen.

• Platelets form a clot on top, initiating thrombus formation.

• Macrophages get trapped, enlarging the clot and obstructing blood flow, leading to ischemia.

• Unstable clots can dislodge and travel to the heart (causing myocardial infarction), lungs (causing pulmonary embolism), or brain (causing stroke).

Hypertension

• High blood pressure; a major risk factor for heart disease, stroke, and kidney failure.

• Risk of cardiovascular disease doubles with each 20/10 mmHg increase in blood pressure above the normal range (120/80 mmHg).

• Types:

  • Essential Hypertension: No clear cause (90% of cases); normal cardiac output but increased peripheral resistance; often associated with lifestyle factors.

  • Secondary Hypertension: Has an identifiable cause that can be fixed (e.g., kidney disease, endocrine disorders, sleep apnea).