Chapter 20 Cardiovascular System_Vessels Circulation

Structure & Function of Blood Vessels

• Three types of blood vessels:
  • Arteries: convey blood from the heart to capillaries.
  • Capillaries: microscopic porous blood vessels; exchange substances between blood and tissues.
  • Veins: transport blood from capillaries to the heart.

General Structure of Vessels

• Vessel composition:
  • Lumen: space inside the vessel.
  • Walls composed of three layers called tunics: tunica intima, tunica media, and tunica externa.
• Tunics:
  • Tunica intima:
    • Innermost layer of the vessel wall.
    • Endothelium of simple squamous epithelium.
  • Tunica media:
    • Middle layer of the vessel wall.
    • Circularly arranged layers of smooth muscle cells with elastic fibers.
    • Contraction causes vasoconstriction, narrowing the lumen.
    • Relaxation causes vasodilation, widening the lumen.
  • Tunica externa:
    • Outermost layer of the vessel wall.
    • Areolar connective tissue with elastic and collagen fibers.
    • Helps anchor the vessel to other structures.
    • May contain vasa vasorum: small arteries required to supply very large vessels.
• Comparison of different vessel types:
  • Companion vessels lie next to each other (arteries and veins serving the same body region).
  • Arteries:
    • Have a thicker tunica media and a narrower lumen than veins.
    • Have more elastic and collagen fibers, allowing them to spring back to shape.
    • More resilient and resistant to changes in blood pressure.
  • Veins:
    • Have a thicker tunica externa and a larger lumen than arteries.
    • Have fewer elastic and collagen fibers; the wall collapses if there is no blood in the vessel.
  • Capillaries:
    • Contain only the tunica intima (no subendothelial layer).
    • Composed of endothelium and basement membrane.
    • A thin wall allows for rapid gas and nutrient exchange.

Arteries

• Artery branching:
  • Branch into smaller vessels extending from the heart.
  • Decrease in lumen diameter and elastic fibers.
  • Increase in the relative amount of smooth muscle.
  • Three basic types: elastic arteries, muscular arteries, and arterioles.
• Elastic (conducting) arteries:
  • Largest arteries, with diameters from 2.5 to 1 cm.
  • Conduct blood from the heart to muscular arteries.
  • Have a large proportion of elastic fibers, allowing for stretch and recoil, which helps propel blood during diastole.
  • Examples: aorta, pulmonary trunk, common carotid, and common iliac arteries.
• Muscular (distributing) arteries:
  • Medium arteries, with diameters from 1 cm to 3 mm.
  • Distribute blood to specific body regions.
  • Muscle allows vasoconstriction and dilation.
  • Elastic tissue in two layers:
    • Internal elastic lamina between the tunica intima and tunica media.
    • External elastic lamina between the tunica media and tunica externa.
  • Most named arteries, e.g., brachial artery and coronary arteries.
• Arterioles:
  • Smallest arteries, with diameters of 3 mm to 10 micrometers.
  • Larger arterioles have three tunics.
  • Smaller arterioles have only a thin endothelium and a single layer of smooth muscle.
  • Smooth muscle is usually somewhat constricted, called vasomotor tone, which is regulated by the vasomotor center in the brainstem.
  • Regulate systemic blood pressure and blood flow.

Clinical View: Atherosclerosis

• Progressive disease of elastic and muscular arteries.
• Presence of atheroma (atheromatous plaque):
  • Thickening of the tunica intima, narrowing the arterial lumen.
  • May be due to response to injury to endothelium caused by infection, trauma, or hypertension, resulting in inflammation and atheroma formation.
  • Unaware of plaques until they restrict blood flow to a region.
• Increased cholesterol in the blood (hypercholesterolemia) makes one prone to the disease.
• Males are more affected than females.
• Smoking and hypertension increase vascular injury and overall risk.
• Treatment:
  • Angioplasty to expand the narrowed region of the artery.
  • Coronary bypass surgery.

Clinical View: Aneurysm

• Part of the arterial wall thins and balloons out, making it more prone to rupture, which can cause massive bleeding and death.
• Elastic and muscular arteries become less able to withstand forces from pulsating blood with age.
• Risk increases with age.
• Most common in the aorta or arteries at the base of the brain.

Capillaries

• Small vessels connecting arterioles to venules.
• Average length = 1 mm; diameter = 8 to 10 micrometers; erythrocytes travel single file (rouleau).
• The wall consists of an endothelial layer on the basement membrane.
• A thin wall and small diameter are optimal for exchange between blood and tissue fluid.
• Three types: continuous, fenestrated, and sinusoid.
• Continuous capillaries:
  • Endothelial cells form a continuous lining.
  • Tight junctions connect cells but do not form a complete seal; intercellular clefts are gaps between endothelial cells of the capillary wall.
  • Large particles (e.g., cells, proteins) cannot pass, but smaller molecules (e.g., glucose) can pass through the wall.
  • Common: found in muscle, skin, lungs, and the central nervous system.
• Fenestrated capillaries:
  • Endothelial cells form a continuous lining, but the cells have fenestrations (pores).
  • Fenestrations allow movement of smaller plasma proteins.
  • Found in areas where much fluid transport happens, e.g., intestine capillaries absorbing nutrients and kidney capillaries filtering blood to form urine.
• Sinusoids (discontinuous capillaries):
  • Endothelial cells form an incomplete lining with large gaps.
  • Basement membrane is incomplete or absent.
  • Openings allow the transport of large substances (formed elements, large proteins).
  • Found in bone marrow, the spleen, and some endocrine glands.
• Capillary beds:
  • Groups of capillaries functioning together.
  • Fed by a metarteriole (a vessel branch of an arteriole).
    • Proximal part encircled by scattered smooth muscle cells.
    • Distal part, thoroughfare channel, has no smooth muscle cells and connects to the postcapillary venule, draining the bed.
  • True capillaries:
    • Vessels branching from the metarteriole, which make up the bulk of the capillary bed.
  • Precapillary sphincter:
    • Smooth muscle ring at the true capillary origin.
    • Sphincter relaxation permits blood to flow into true capillaries.
    • Sphincter contraction causes blood to bypass the capillary bed.
    • Vasomotion: cycle of contracting and relaxing precapillary sphincters.
    • At any time, only one-quarter of the body’s capillary beds are open.
  • Perfusion:
    • Amount of blood entering capillaries per unit time per gram of tissue.
    • Units are mL/min/g.

Veins

• Venules:
  • Smallest veins, with diameters of 8 to 100 micrometers.
  • Companion vessels with arterioles.
  • Smallest venules are postcapillary venules.
  • Largest venules having all three tunics merge to form veins.
• Small and medium-sized veins:
  • Companion vessels with muscular arteries.
• Largest veins:
  • Travel with elastic arteries.
• Most veins of these sizes have numerous valves to prevent blood from pooling in the limbs and ensure flow toward the heart.
  • Valves are made of the tunica intima with elastic and collagen fibers and have a similar structure to the heart’s semilunar valves.
• Systemic veins as blood reservoirs:
  • At rest: 70% of blood in systemic circulation:
    • Systemic veins: 55%
    • Systemic arteries: 10%
    • Systemic capillaries: 5%
  • Pulmonary circulation has 18% of the blood.
  • The heart has 12% of the blood.
  • Blood can be moved from veins into circulation via vasoconstriction of veins, e.g., when more blood is needed during exertion.
  • Blood can be shifted back into reservoirs via vasodilation, e.g., when less blood is needed during rest.

Pathways of Blood Vessels

• Simple pathway:
  • One major artery delivers blood to an organ or region.
    • An end artery is one that provides only one path for blood to reach an organ or region.
    • It branches into smaller arteries that become arterioles.
  • Each arteriole feeds into a capillary bed.
  • The capillary bed is drained by a venule.
  • Venules merge to one major vein.
  • E.g., a splenic artery delivers blood to the spleen, and the splenic vein drains the organ.
• Alternative pathways are configured differently:
  • Arterial anastomosis (arterial joining):
    • Two or more arteries converge to supply the same region, e.g., superior and inferior epigastric arteries supplying the abdominal wall.
    • If the junction is small, the arteries might be functional end arteries.
  • Venous anastomosis are more common:
    • Two or more veins drain the same body region, e.g., basilic, brachial, and cephalic veins draining the upper limb.
  • Arteriovenous anastomosis (shunt):
    • Transports blood from the artery directly to the vein, e.g., in fingers, toes, palms, and ears.
    • Allows areas to be bypassed if the body is hypothermic.
  • Portal system (two capillary beds in sequence):
    • Path: artery → capillary bed → portal vein → capillary bed → vein, e.g., the hypothalamo-hypophyseal portal system.

Total Cross-Sectional Area & Blood Flow Velocity

• Cross-sectional area of one vessel is the lumen diameter.
• Total cross-sectional area is the sum of the diameters of all vessels of a certain type (artery, capillary, or vein).
  • Collectively, the total cross-sectional area of capillaries is the largest because there are so many capillaries.
• Blood flow velocity is inversely related to the total cross-sectional area.
  • Blood flow is slow in capillaries, allowing for exchange between blood and tissue fluid.

Diffusion & Vesicular Transport

• Diffusion: substances leave or enter the blood according to their concentration gradient (high to low concentration).
  • Oxygen, hormones, and nutrients move from blood to interstitial fluid.
  • Carbon dioxide and wastes diffuse from tissue to blood.
• The route diffusion takes depends on particle size.
  • Small solutes (e.g., O_2) can diffuse through endothelial cells or intercellular clefts.
  • Larger solutes (e.g., some proteins) pass through fenestrations or gaps in sinusoids.
• Vesicular transport:
  • Endothelial cells use pinocytosis and exocytosis.
    • Take substances in by pinocytosis to form fluid-filled vesicles at the plasma membrane.
    • Transport vesicle across the cell.
    • Secrete substance from the other side by exocytosis.
    • This process is used in both directions (both to and from the blood).
    • Certain hormones and fatty acids are transported by this method.

Bulk Flow

• Fluid and small solutes flow easily through the capillary’s openings; large solutes are blocked.
  • Filtration: Fluid moves out of blood; occurs on the arterial end of the capillary.
  • Reabsorption: Fluid moves back into blood;occurs on the venous end.
• Bulk flow: fluids flow down the pressure gradient, and large amounts of fluids and dissolved substances move.
  • Movement direction depends on the net pressure of opposing forces: hydrostatic pressure versus colloid pressure.
  • Hydrostatic pressure: force exerted by a fluid.
    • Blood hydrostatic pressure (HP_b): force exerted per unit area by blood on the vessel wall, which promotes filtration from the capillary.
    • Interstitial fluid hydrostatic pressure (HP_{if}): force of interstitial fluid on the outside of the blood vessel, which is close to zero in most tissues.
  • Colloid osmotic pressure: the pull on water due to the presence of protein solutes.
    • Blood colloid osmotic pressure (COP_b): draws fluid into blood due to blood proteins (e.g., albumins), which promotes reabsorption (opposes the dominant hydrostatic pressure); clinically called oncotic pressure.
    • Interstitial fluid colloid osmotic pressure (COP_{if}): draws fluid into interstitial fluid; since few proteins are present in interstitial fluid, this is relatively low (0 to 5 mm Hg).
• Net filtration pressure (NFP):
  • NFP is the difference between net hydrostatic pressure and net colloid osmotic pressure:
  • NFP = (HPb - HP{if}) - (COPb - COP{if})
  • Net hydrostatic pressure = difference between blood and interstitial fluid hydrostatic pressures.
  • Net colloid osmotic pressure = difference between blood and interstitial fluid osmotic pressures.
  • NFP changes along the length of a capillary; it is higher at the arterial end than at the venous end.
    • At the arterial end, NFP favors filtration:
      • HPb = 35 mm Hg; HP{if} = 0; COPb = 26 mm Hg; COP{if} = 5 mm Hg.
      • NFP = (35 - 0) - (26 - 5) = 14 mm Hg.
    • At the venous end, NFP favors reabsorption:
      • The venous end of the capillary has less blood in it as some has filtered out.
      • HPb = 16 mm Hg; HP{if} = 0; COPb = 26 mm Hg; COP{if} = 5 mm Hg.
      • NFP = (16 - 0) - (26 - 5) = -5 mm Hg.

Role of the Lymphatic System

• The lymphatic system:
  • Picks up excess fluid not reabsorbed at the venous capillary end (15% of fluid not reabsorbed by the capillary).
  • Filters the fluid and returns it to venous circulation.

Local Blood Flow

• Not all capillaries are filled simultaneously; local blood flow varies.
• Flow is measured in milliliters per minute and must be high enough to maintain adequate perfusion.
• Local blood flow is dependent on:
  • The degree of tissue vascularity.
  • The myogenic response.
  • Local regulatory factors altering blood flow.
  • Total blood flow.

Degree of Vascularization & Angiogenesis

• Degree of vascularization: extent of vessels in a tissue.
  • Metabolically active tissues have high vascularity, e.g., the brain, skeletal muscle, heart, and liver.
  • Other structures have little vascularity or are avascular: tendons, ligaments, epithelia, cartilage, the cornea, and the lens of the eye.
• Angiogenesis: formation of new vessels, which occurs over weeks to months to increase potential perfusion.
  • Examples:
    • In skeletal muscle in response to aerobic training.
    • In adipose tissue with weight gain.
    • In coronary vessels in response to gradual blockage.
• Regression: return to the previous state of blood vessels.
  • Examples of when vessels regress:
    • In skeletal muscle after an individual becomes sedentary.
    • In adipose tissue when weight is lost.

Clinical View: Tumor Angiogenesis

• Since cancer cells require oxygen and nutrients, they trigger the growth of new vessels as the tumor grows.
• Cancer cells secrete molecules that cause host cells to release growth factors.
• Research is looking for a way to stop this and starve the tumor.

Myogenic Response

• Myogenic response: smooth muscle in the blood vessel wall keeps local flow relatively constant.
  • If systemic blood pressure rises and more blood enters an arteriole, it will stretch.
    • The smooth muscle of the arteriole wall will respond by contracting to return local flow to original levels.
  • If systemic blood pressure decreases and the amount of blood decreases, there will be less stretch.
    • In response to decreased stretch, smooth muscle of the vessel relaxes to return local blood flow to original levels.

Local, Short-Term Regulation

• Blood flow is locally regulated to meet tissue needs and changes when metabolic activity changes or tissue is damaged.
• Vasoactive chemicals alter blood flow.
  • Vasodilators dilate arterioles and relax precapillary sphincters, increasing flow into capillary beds.
  • Vasoconstrictors constrict arterioles and cause contraction of precapillary sphincters, decreasing flow into capillary beds.
• Autoregulation and changing metabolic activity:
  • The process by which tissue controls local blood flow.
  • When tissue activity increases, varied stimuli signal inadequate perfusion and act as vasodilators.
    • Oxygen and nutrient levels decline.
    • Carbon dioxide, lactic acid, H^+, and K^+ increase.
  • Negative feedback: as perfusion increases, vessels constrict in response.
• Reactive hyperemia: increase in blood flow after it is temporarily disrupted.
  • Additional blood is required to resupply oxygen and nutrients and eliminate wastes, e.g., entering a warm room after being in the cold.
    • Dermis blood vessels are constricted in the cold to conserve heat.
    • Blood flow increases after entering a warm room.
• Short-term flow regulation due to tissue damage or as part of the body’s defenses:
  • Inflammation:
    • Damaged tissue, leukocytes, and platelets release vasoactive chemicals, e.g., histamine and bradykinin, which cause arterioles to dilate.
    • Released in response to trauma, allergy, infection, or exercise.
    • May also stimulate the release of nitric oxide, another vasodilator.
  • Tissue damage can also lead to the release of vasoconstrictors, e.g., prostaglandins and thromboxanes, to help prevent blood loss through damaged vessels.

Relationship of Local & Total Blood Flow

• Total blood flow:
  • The amount of blood transported through the vasculature per unit of time, which is equal to cardiac output (about 5.25 L/min at rest).
  • May increase significantly with exercise, making more blood available to tissues.
  • Regulation of total flow depends on both the heart and the vessels.

Blood Pressure

• Blood pressure: force of blood against the vessel wall.
  • Blood pressure gradient: change in pressure from one end of the vessel to the other, which propels blood through the vessels.
    • Pressure is highest in arteries and lowest in veins.
• Arterial blood pressure:
  • Blood flow in arteries pulses with the cardiac cycle.
    • Systolic pressure: occurs when the ventricle contracts (systole), which is the highest pressure generated in arteries (they are stretched) and is recorded as the upper number of the blood pressure ratio (e.g., systolic pressure is 120 mm Hg if blood pressure is 120/80).
    • Diastolic pressure: occurs when ventricles relax (diastole), which is the lowest pressure generated in arteries (they recoil) and is recorded as the lower number of the blood pressure ratio (e.g., diastolic pressure is 80 mm Hg if blood pressure is 120/80).
  • Pulse pressure: pressure in arteries added by heart contraction, which equals the difference between systolic and diastolic blood pressure (e.g., pulse pressure = 40 mm Hg if blood pressure is 120/80); it reflects the elasticity and recoil of arteries.
    • These tend to decline with age and disease.
    • Pulse pressure allows for palpation of a throbbing pulse in elastic and muscular arteries.
• Pulse: throbbing of the arterial wall that allows determination of heartbeat.
  • More forceful pulse associated with higher pressure.
  • Absence indicates flow to a body part is lacking.
  • Pulse points are where the artery may be compressed against a solid structure, e.g., radial, common carotid, femoral, and dorsalis pedis.
• Mean arterial pressure (MAP): average arterial blood pressure across the entire cardiac cycle.
  • Since diastole lasts longer than systole, the mean is weighted to be closer to diastolic pressure:
    • MAP = diastolic pressure + 1/3 pulse pressure
    • E.g., if blood pressure is 120/80, MAP = 80 + 40/3 = 93.
  • Provides an index of perfusion.
    • E.g., MAP < 60 may indicate insufficient blood flow.
• Capillary blood pressure:
  • Pressure no longer fluctuates between systolic and diastolic; flow and pressure are smooth.
  • Needs to be high enough for the exchange of substances but low enough not to damage vessels.
  • The arterial end of the capillary is at about 40 mm Hg, and the venous end of the capillary is below 20 mm Hg.
    • Accounts for filtration and reabsorption at respective ends.
• Cerebral edema: excess interstitial fluid in the brain, which can occur if MAP is greater than 160 mm Hg, increasing filtration in brain capillaries.
  • No lymph vessels here, so accumulation of excess fluid.
• Venous blood pressure:
  • Venous return of blood to the heart depends on pressure gradient, the skeletal muscle pump, and the respiratory pump.
  • Venous pressure is low and not pulsatile.
  • The pressure gradient is small: BP is 20 mm Hg in venules and almost 0 in the vena cava.
  • The skeletal muscle pump assists venous return from limbs:
    • As the muscle contracts, veins are squeezed, and blood is pushed.
    • Valves prevent backflow.
    • Blood is moved more quickly during exercise.
    • Blood pools in leg veins with prolonged inactivity.
  • The respiratory pump assists venous return in the thorax.
    • Both inspiration and expiration cause pressure gradient changes that help.
    • In inspiration: the diaphragm contracts, so abdominal pressure increases and thoracic pressure decreases, and blood in abdominal veins is driven toward the thoracic cavity.
    • In expiration: the diaphragm relaxes, so thoracic pressure increases while abdominal pressure decreases, and blood in thoracic cavity veins is driven toward the heart, while blood in lower limbs is allowed into abdominal veins.
    • Increases in breathing rate facilitate blood movement.

Clinical View: Deep Vein Thrombosis

• Clot (thrombosis) in a vein and most common site is the calf.
• Heart disease, immobility, and risk factors can lead to:
  - fever,
  - tenderness,
  - redness,
  - pain, and
  - swelling in areas drained and a rapid heartbeat.
• Pulmonary embolus is the most serious complication, where a clot breaks free and lodges in the pulmonary artery, which can cause respiratory failure and death.

Clinical View: Varicose Veins

• Dilated and tortuous with nonfunctional valves causing blood pooling.
• Most common in superficial veins of lower limbs.
• Result of genetics, aging, extended standing, obesity, and pregnancy.
• In the anorectal region, hemorrhoids are due to increased abdominal pressure.

Blood Pressure Gradient in the Systemic Circulation

• The systemic gradient is the difference between pressure in arteries near the heart and in the vena cava.
  • Mean blood pressure in arteries: 93 mm Hg.
  • Blood pressure in the vena cava: 0.
  • Blood pressure gradient: 93 mm Hg, which is the driving force to move blood through vasculature.
  • Increasing gradient increases total blood flow.
  • The gradient is increased by increased cardiac output.

Clinical View: Circulatory Shock

• Insufficient blood flow to perfuse tissues, which can be due to impaired heart or low venous return from:
  - hemorrhage,
  - dehydration, or
  - an allergic reaction, or
  - an obstructed vein, or
  - venous pooling from
  • prolonged immobility or
  • extensive vasodilation from
    1. bacterial toxins or brainstem trauma causing a loss of vasomotor tone.

Resistance

• Resistance: the friction blood encounters due to contact between blood and the vessel wall, which opposes blood flow.
  • Peripheral resistance is resistance of blood in blood vessels (as opposed to the heart) and is affected by:
    viscosity, vessel length, and lumen size.
    • Vessel length: longer vessels create more resistance since friction occurs along the length of the vessel, which normally stays constant, but weight gain or loss changes vessel length.
      • Weight gain is associated with angiogenesis (increased resistance), and weight loss is associated with vessel regression (decreased resistance).
    • Blood viscosity: resistance of fluid to its flow, where greater thickness is greater viscosity, which raises resistance and depends on the percentage of particles in fluid.
      • Blood has formed elements and proteins and is about 5 times more viscous than water.
      • Viscosity decreases with anemia (low blood cell count) and increases with blood doping (high cell count) or with dehydration (a greater percentage of cells).
    • Vessel radius: a smaller radius creates more resistance.
      • Blood has laminar flow: different flow rate within the vessel, where flow is fast in the center of the lumen but slower near the vessel wall, where the vessel wall creates resistance.
      • As the diameter increases, resistance decreases and flow increases, with relatively less blood flowing along the vessel wall with dilation.
        - Flow is proportional to the radius to the fourth power:
        F \propto r^4.
        - E.g., the radius increases 1 mm to 2 mm; the change in flow is 16 times greater.
        - Changing radius is the main way resistance is regulated, and arteriole radius usually regulates resistance, where vasodilation and vasoconstriction are controlled by the sympathetic division of the ANS. Big changes in total resistance are from small diameter changes.
        - Resistance is increased in atherosclerosis.

Relationship of Blood Flow to Blood Pressure Gradients & Resistance

• Total blood flow: the amount of blood moving through the system per unit time.
  • Flow is proportional to the pressure gradient divided by resistance:
    F \propto \frac{\Delta P}{R}.
    - Systemic blood pressure gradient = \Delta P.
    - As the gradient increases, total blood flow increases, and the gradient is generally increased by increasing cardiac output.
• Resistance = R.
  - As resistance increases, total blood flow decreases, and resistance can be increased by increasing blood viscosity, increasing vessel length, or decreasing vessel lumen diameter.
• Systemic blood pressure and resistance:
  • Clinical conditions leading to sustained increased resistance elevate blood pressure, e.g., obesity or atherosclerosis, which requires the heart to work harder to overcome higher resistance.

Regulation of Blood Pressure & Blood Flow

• Blood pressure must be kept in the proper range:
  • High enough to maintain tissue perfusion but not so high as to damage vessels.
  • Pressure depends on
    cardiac output, resistance, and blood volume, and these variables are regulated by the nervous and endocrine systems.

Neural Regulation of Blood Pressure

• Autonomic reflexes regulate blood pressure short-term, and involve nuclei in the medulla oblongata, quickly adjusting cardiac output, resistance, or both, to meet momentary pressure needs (e.g., standing up).
• The cardiovascular center of the medulla contains two autonomic nuclei: cardiac center & vasomotor center:
  • The cardiac center influences blood pressure by influencing cardiac output.
  • The vasomotor center influences blood pressure by influencing vessel diameter (vessel constriction influences resistance).
• The cardiac center houses two nuclei:
  • Cardioinhibitory center is the origin of parasympathetic pathways.
  • Extend to the SA and AV nodes.
  • Activity decreases heart rate and slows the conduction of electrical signals, which decreases cardiac output and blood pressure.
  • Cardioacceleratory center is the origin of sympathetic pathways.
  • Paths extend to the sinoatrial (SA) node and myocardium.
  • Activity increases heart rate and force of contraction, which increases cardiac output and blood pressure.
  • The vasomotor center is the origin of sympathetic pathways.
    • Pathways extend from here to blood vessels, where they release norepinephrine (NE).
      • Sympathetic activation also stimulates the adrenal medulla to release epinephrine (EPI) and NE as hormones.
    • Most blood vessels’ smooth muscle cells have α1 receptors, where NE and EPI cause vessel constriction.
    • Some blood vessels’ smooth muscle cells have β2 receptors, and NE and EPI cause vasodilation in response to stimulation.
      Sympathetic activation & adrenal secretion lead to:
    • Increased peripheral resistance and blood pressure, where more blood vessels are stimulated to constrict than to dilate.
    • Larger circulating blood volume and increased blood pressure, where vasoconstriction of veins shifts blood from venous reservoirs.
    • Redistribution of blood flow, where more blood goes to skeletal muscles and the heart and less blood to most other structures.
    • Inhibition of the sympathetic division reverses the above changes.
  • Baroreceptors: nerve endings that respond to stretch of a vessel wall, and their firing rate changes with blood pressure changes.
    • Located in the tunica externa of the aortic arch and carotid sinuses.
      • Aortic arch baroreceptors transmit signals to the cardiovascular center through the vagus nerve (CN X) and are important in regulating systemic blood pressure.
      • Carotid sinuses transmit nerve signals to the cardiovascular center via the glossopharyngeal nerve (CN IX).
        • Monitor blood pressure in the head and neck (vessels that serve the brain) and are more sensitive to blood pressure changes than aortic arch receptors.
  • Autonomic reflexes for blood pressure are baroreceptor reflexes.
    • Initiated by a decrease or increase in blood pressure.
    • If blood pressure decreases:
      • Vessel stretch declines, and the baroreceptor firing rate decreases.
      • This activates the cardioacceleratory center to stimulate the sympathetic pathways to increase cardiac output.
      • It inhibits the cardioinhibitory center to minimize parasympathetic activity.
      • It activates the vasomotor center to stimulate the sympathetic pathways to increase vasoconstriction.
• The increase in cardiac output and resistance raises blood pressure.
  - If blood pressure increases:
  - Vessel stretch and baroreceptor firing rate increase.
  - This causes the cardioacceleratory center to send fewer signals along sympathetic pathways.
  - It stimulates the cardioinhibitory center to activate parasympathetic pathways to the SA and AV nodes of the heart.
  - It causes the vasomotor center to send fewer signals along the sympathetic pathways to blood vessels.
• The decrease in cardiac output and resistance lowers blood pressure.
  - Baroreceptor reflexes are best for quick changes in BP, but are ineffective for long-term BP regulation.
  Chemoreceptor reflexes also influence blood pressure.
  - Stimulation of chemoreceptors brings about negative feedback reflexes to return blood chemistry to normal, with responses in respiratory and cardiovascular systems.
  - The main peripheral chemoreceptors are in aortic and carotid bodies.
  - Both send input to the cardiovascular center.
  - Aortic bodies are in the aortic arch and send signals via the vagus nerve.
  - Carotid bodies are at the bifurcation of the common carotid artery and send signals via the glossopharyngeal nerve.
• High carbon dioxide, low pH, and very low oxygen stimulate chemoreceptors and stimulate the vasomotor center.
  - Chemoreceptor firing stimulates the vasomotor center, increasing nerve signals along sympathetic pathways to vessels, shifting blood from venous reservoirs to increase venous return, which raises blood pressure and increases blood flow (including pulmonary), allowing for increased respiratory gas exchange in the lungs.
• Higher brain centers:
  - The hypothalamus can increase cardiac output and resistance, causing a result might be increased body temperature or a fight-or-flight response.
  - The limbic system can alter blood pressure in response to emotions or memories.

Hormonal Regulation of Blood Pressure

• Hormones also regulate blood pressure.
  - Epinephrine and norepinephrine work with the sympathetic nervous system.
  - Angiotensin II, antidiuretic hormone, aldosterone, and atrial natriuretic peptide also have effects.
  - Influence pressure through effects on resistance, blood volume, or both.
• Renin-angiotensin system: - The liver makes inactive angiotensinogen protein and releases it into the blood. - The kidneys release renin into the blood in response to low BP or sympathetic nervous system activity. - Renin converts angiotensinogen to angiotensin I in blood. - Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II, and the enzyme is located in the capillaries of the lung. Angiotensin II raises blood pressure. - Acts as a powerful vasoconstrictor (raises resistance). - Stimulates the thirst center, and fluid intake increases blood volume. - Acts on kidneys to decrease urine formation, lessening fluid lost from the blood and maintaining blood volume. - Stimulates the release of aldosterone and antidiuretic hormone.
  • Aldosterone helps maintain blood volume and pressure.
    -Released from the adrenal cortex and release is triggered by several stimuli, including angiotensin II.
    -Increases absorption of sodium ions and water in the kidney, which decreases urine output. Anti-diuretic hormone (ADH) helps maintain and elevate blood pressure. Released from the posterior pituitary and the release is triggered by nerve signals from the hypothalamus stimulated by increased blood concentration or angiotensin II. ADH Effects:
    • Increases water reabsorption in kidney (less fluid loss, maintains blood volume).
    • Stimulates thirst center to increase fluid intake (raising blood volume).
    • In large amounts it causes vasoconstriction (increasing resistance and pressure).
    - Because of ADH it is sometimes termed vasopressin.
    • Atrial natriuretic peptide decreases blood pressure.
      -Released from atria of the heart when walls are stretched by high blood volume.
      -Stimulates