Anatomy & Physiology 11: Blood Vessels and Regulation

Progression and Structure of the Systemic Circuit

  • Progression of Vessels through the Systemic Circuit: Blood moves from the heart through a series of vessels with varying structures and functions in the following order:

    • Elastic Arteries: The largest, most resilient arteries (e.g., aorta) that can withstand high pressure changes.

    • Muscular Arteries: Medium-sized vessels that distribute blood to skeletal muscles and internal organs.

    • Arterioles: Smallest arterial branches that lead into capillary beds.

    • Capillaries: The site of exchange between blood and interstitial fluid.

    • Venules: Smallest venous vessels that collect blood from capillaries.

    • Medium-sized Veins: Vessels containing valves to prevent backflow.

    • Large Veins: The final vessels (e.g., venae cavae) returning blood to the heart.

  • Histological Layers (Tunicae):

    • Tunica Intima (Inner Layer): Includes the endothelial lining , endothelium , simple squamous epithelium, and contacts the blood and a surrounding layer of connective tissue with a variable number of elastic fibers.

    • Tunica Media (Middle Layer): Contains concentric sheets of smooth muscle tissue in a framework of loose connective tissue. It is responsible for changing the vessel diameter.

    • Tunica Externa (Outer Layer): A connective tissue sheath overall; in arteries, it contains collagen fibers with scattered bands of elastic fibers, while in veins, it is generally thicker than the tunica media.

  • Elastic Membranes:

    • Internal Elastic Membrane: Located in the outer margin of the tunica intima of arteries. ( between tunica intima and media)

    • External Elastic Membrane: Located between the tunica media and the tunica externa in arteries.

  • Vascular Smooth Muscle Dynamics:

    • Vasodilation: If smooth muscle cells in the tunica media of an artery relax, the lumen of the artery increases in diameter.

    • Vasoconstriction: If smooth muscle cells in the tunica media contract, the lumen of the artery decreases in diameter.

  • Nutrient Supply to Vessel Walls:

    • Vasa Vasorum: The cells of the tunica media and tunica externa in large vessels are too far from the lumen to receive nutrients by diffusion; they are nourished by the vasa vasorum ("vessels of vessels"), which are small arteries and veins located in the walls of the larger vessels.

  • Artery vs. Vein Microscopic Comparison:

    • Arteries: Usually maintain a circular or oval shape in cross-section because their walls are thick and strong. They have smaller lumens compared to veins and thicker tunica media layers.

    • Veins: Often appear flattened or collapsed in section because their walls are thinner and less resilient. They have larger lumens and thinner tunica media.

Vessel Characteristics and Capillary Exchange

  • Contractile/Muscular and Elastic Vessel Groups:

    • Elastic Arteries: ALSO CALLED CONDUCTING ARTERIES.Considered the "elastic" vessels because they stretch and recoil with the heartbeat. Pulse Force

      Heart contracts → artery stretches

      Heart relaxes → artery recoils

      This recoil keeps blood moving forward continuously.

    • Function- The primary function of elastic artery is to smooth out pulse pressure. They expand and recoil to maintain blood flow during the cardiac cycle.

    • Muscular Arteries ALSO KNOWN AS DISTRIBUTION ARTERIES : Most common artery type.

      Function:

      Distribute blood to organs

      Regulate blood pressure

      Contain:

      More smooth muscle

      Less elastin

      Considered the "contractile" or "muscular" vessels because they contain a high proportion of smooth muscle compared to elastic tissue.

Arterioles

Smallest arteries

thin or incomplete tunica media and little or no tunica externa.

Resistance vessels.

Why?

Small diameter changes create huge changes in resistance.

Local tissues can control them.

Example:

Low oxygen in tissue →

Arteriole dilates →

More blood enters tissue

  • Aneurysms:

    • Definition: An aneurysm is a bulge in the weakened wall of an artery.

    • Effects of Bursting: If an aneurysm bursts, it leads to massive internal bleeding (hemorrhage), which can be fatal, especially in the brain or aorta.

  • Types of Capillaries and Exchange Mechanisms:

    • Fenestrated Capillaries: These have pores (fenestrae) in their endothelial lining. They allow for the rapid exchange of water and solutes (such as small peptides or nutrients) to leave or enter the blood.

    • Sinusoids (Sinusoidal Capillaries): These allow for the exchange of large substances like plasma proteins and blood cells. They feature large gaps and a thin or absent basal lamina, which permits these large molecules to pass through.

    • Continuous Capillaries: These allow for the exchange of respiratory gases (O2O_2 and CO2CO_2). These gases cross in and out of the blood via simple diffusion across the phospholipid membranes of the endothelial cells.

  • Vessel Physiology Definitions:

    • Vasomotion: The rhythmic changes in vessel diameter (alternating contraction and relaxation) of the precapillary sphincters that cause blood flow in capillaries to occur in pulses rather than a steady stream.

    • Precapillary Sphincters: Bands of smooth muscle at the entrance to each capillary that guard the opening and regulate blood flow into the capillary bed.

    • Collaterals: Multiple arteries that supply the same capillary bed; this ensures that if one artery is blocked, the tissue still receives blood (arterial anastomosis).

  • Capacitance Vessels (Veins):

    • Definition: Veins are called capacitance vessels because they can expand easily to store large volumes of blood at low pressure.

    • Blood Volume Distribution: Approximately 64%64\% of total blood volume is located in the systemic venous system at any given time.

    • Response to Blood Loss: In the event of serious hemorrhaging, the vasomotor center in the medulla oblongata stimulates sympathetic nerves, leading to venoconstriction. This reduces the volume of the venous system and shifts blood into the arterial system to maintain pressure.

Hemodynamics and Total Peripheral Resistance

  • Blood Flow Relationships:

    • Capillary blood flow is proportional to PressureResistance\frac{\text{Pressure}}{\text{Resistance}}.

    • Change in Pressure: If pressure increases, blood flow increases.

    • Change in Resistance: If resistance increases, blood flow decreases.

  • Total Peripheral Resistance (TPR):

    • Variables Affecting TPR:

      1. Vascular Resistance: Friction between blood and vessel walls (determined by vessel length and vessel diameter).

      2. Blood Viscosity: The "thickness" or resistance to flow of the blood itself.

      3. Turbulence: Upsetting the smooth flow of blood due to high flow rates, irregular surfaces, or sudden changes in diameter.

    • Greatest Effect Factor: Blood vessel diameter (specifically in small arterioles) has the most significant influence on total peripheral resistance.

  • Atherosclerosis:

    • Definition: Atherosclerosis is the buildup of fatty plaques

    • (atheromas) along the inner walls of arteries.

    • Effect on TPR: It increases total peripheral resistance by narrowing the vessel lumen and increasing turbulence.

  • Velocity of Blood Flow:

    • Blood flow velocity is inversely related to the total cross-sectional area of the vessels.

    • Velocity is highest in the aorta, decreases significantly as blood moves toward the capillaries (where total cross-sectional area is highest), and increases again as blood moves from the venules back to the heart.

  • Arterial Blood Pressure:

    • Systolic Pressure (Peak): The peak arterial blood pressure attained during ventricular contraction.

    • Diastolic Pressure (Minimum): The minimum arterial pressure reached at the end of ventricular relaxation.

    • Mean Arterial Pressure (MAP) Calculation:     MAP=Diastolic Pressure+13(Systolic Pressure−Diastolic Pressure)MAP = \text{Diastolic Pressure} + \frac{1}{3}(\text{Systolic Pressure} - \text{Diastolic Pressure})

    • Hypotension: Abnormally low blood pressure.

    • Hypertension: Abnormally high blood pressure.

  • Venous Return Factors:

    • Assistance Mechanisms: Venous return is assisted by the skeletal muscle pump (muscle contractions squeezing veins) and the respiratory pump (pressure changes in the thoracic cavity during breathing).

    • Need for Assistance: Assistance is necessary because venous pressure is very low (18 mm Hg18\,mm\,Hg to approximately 2 mm Hg2\,mm\,Hg), and it must overcome gravity to return blood to the heart from the lower extremities.

Capillary Exchange Dynamics and Regulation

  • Filtration and Reabsorption:

    • Filtration: Driven primarily by Capillary Hydrostatic Pressure (CHP). It moves fluids and solutes from the blood (capillary) to the interstitial fluid.

    • Reabsorption: Driven primarily by Blood Colloid Osmotic Pressure (BCOP). It moves fluids and solutes from the interstitial fluid to the blood (capillary).

  • Edema:

    • Definition: Edema is an abnormal accumulation of interstitial fluid in the tissues.

    • Cause: It occurs when the rate of filtration significantly exceeds the rate of reabsorption (e.g., due to high capillary pressure or low plasma proteins) or when lymphatic drainage is blocked.

  • Fluid Balance: During capillary exchange, capillaries typically filter more fluid than they reabsorb (approx. 24 L/day24\,L/day filtered vs 20.4 L/day20.4\,L/day reabsorbed). The excess fluid (3.6 L/day3.6\,L/day) is returned to the cardiovascular system via the lymphatic vessels.

  • Vasoactive Factors:

    • Local Vasodilators: Factors that dilate precapillary sphincters to increase blood flow to a specific part of a tissue. These include:

      1. Decreased oxygen levels (O2O_2).

      2. Increased carbon dioxide levels (CO2CO_2).

      3. Increased hydrogen ion concentration (decreased pH).

      4. Nitric Oxide (NONO) or increased tissue temperature.

    • Local Vasoconstrictors: Compounds that constrict precapillary sphincters to decrease blood flow. Examples include prostaglandins and thromboxanes released by damaged tissues or platelets.

  • Sensory Receptors:

    • Chemoreceptors: Monitor arterial blood for hypoxia (low O2O_2), hypercapnia (high CO2CO_2), and pH changes.

    • Baroreceptors: Monitor changes in blood pressure (stretch) within the vessel walls.

Cardiovascular Regulation: Autoregulation, Neural, and Endocrine

  • Three Levels of Regulation for Tissue Perfusion:

    1. Autoregulation: Local factors make immediate, localized adjustments in blood flow by dilating or constricting precapillary sphincters.

    2. Neural Regulation: The vasomotor center in the medulla oblongata utilizes sympathetic neurons to adjust vessel diameter across large areas of the body.

    3. Endocrine Regulation: Hormones cause long-lasting, systemic changes in BP and volume.

  • Neural Regulation Detail:

    • Increased Vasomotor Output: Sympathetic neurons release more norepinephrine (NENE) onto smooth muscle, causing vasoconstriction.

    • Decreased Vasomotor Output: Sympathetic neurons release less norepinephrine (NENE), causing the muscle to relax, resulting in vasodilation.

  • Baroreceptor Reflexes:

    • Rising Blood Pressure: Increased baroreceptor input to the vasomotor center $\rightarrow$ inhibition of sympathetic neurons $\rightarrow$ peripheral vasodilation $\rightarrow$ decreased BP.

    • Falling Blood Pressure: Decreased baroreceptor input to the vasomotor center $\rightarrow$ stimulation of sympathetic neurons $\rightarrow$ peripheral vasoconstriction (release of NENE) $\rightarrow$ increased BP.

  • Chemoreceptor Reflexes:

    • Activation: Stimulated by increased CO2CO_2 (hypercapnia), decreased pH (acidosis), or decreased O2O_2 (hypoxia).

    • Response: Increased chemoreceptor input stimulates sympathetic neurons to release NENE, causing peripheral vasoconstriction, which increases BP and increases blood flow to the lungs.

  • Endocrine Regulation (BP/Volume Decrease):

    • Epinephrine (Epi) and Norepinephrine (NE): Released from the adrenal medullae; they cause vasoconstriction that increases BP.

    • Renin-Angiotensin System: Renin is released from the kidney in response to low BP, leading to the production of Angiotensin II.

    • Angiotensin II Functions: Causes immediate vasoconstriction (increasing BP) and stimulates the release of Antidiuretic Hormone (ADH) and Aldosterone.

    • ADH and Aldosterone: Work to increase blood volume (ADH promotes water retention; Aldosterone promotes sodium and water retention).

  • Endocrine Regulation (BP/Volume Increase):

    • Atrial Natriuretic Peptide (ANP) and Brain Natriuretic Peptide (BNP): Released from the heart when the walls are overstretched.

    • Effects: These hormones cause increased sodium excretion by the kidneys, increased water loss in urine (diuresis), and peripheral vasodilation.

    • Net Effect: To decrease blood volume and decrease blood pressure.

Every artery and vein has three layers:

  1. Tunica Intima (inner)

    • Endothelium:

      • Simple squamous epithelium.

      • Contacts the blood.

  2. Tunica Media (middle)

    • Smooth muscle.

    • Controls vessel diameter.

  3. Tunica Externa (outer)

    • Connective tissue.

    • Provides protection and anchoring.