CV Homeostasis

Maintaining Homeostasis

Contributing Systems and How Cardiac Output is Maintained

  • Cardiac output is a function of:

    • Heart rate

    • Stroke volume

  • Both heart rate and stroke volume must be maintained to ensure adequate cardiac output.

  • Several endogenous factors contribute to maintaining fluid balance in homeostasis:

    • Autoregulation

    • Neural mechanisms

    • Endocrine control

Autoregulation

  • Definition: Involves chemical signals at the capillary level that trigger constriction or relaxation in response to changes in blood flow.

  • Myogenic response:

    • Reaction to stretching of the arteriole walls due to changes in blood flow.

    • Functions to protect distal smaller, more fragile vessels.

    • Mechanism:

    • Low blood flow: The smooth muscle of the vessels is minimally stretched; in response, it relaxes, allowing dilation and increased blood flow to the tissue.

    • High blood flow: The smooth muscle is more stretched; in response, it constricts, decreasing blood flow to the tissue.

Neural Mechanisms

  • Play a critical role in vascular homeostasis.

  • Include:

    • Cardiovascular (CV) centres in the brain, responsible for regulating cardiac and vascular functions.

    • Generalized neural responses.

    • Autonomic nervous system.

CV Centres in the Brain

  • Location: Medulla oblongata

  • Responses: To changes in:

    • Blood pressure

    • Blood concentrations of O2, CO2, H+

  • Components:

    • Cardioaccelerator centre: Regulates heart rate (HR) and stroke volume (SV) via sympathetic stimulation.

    • Cardioinhibitor centre: Regulates HR and SV via parasympathetic stimulation.

    • Vasomotor centre: Controls vessel tone through the release of norepinephrine.

Baroreceptors

  • Definition: Stretch receptors within vessels and heart chambers that respond to the degree of stretch in the tissue.

  • Role:

    • Sensitive to changes in pressure.

    • Send impulses to the CV centre for the regulation of blood pressure (BP).

  • Location:

    • Aortic sinuses: Walls of ascending aorta.

    • Carotid sinuses: Base of the internal carotid arteries.

Function During Hypertension

  • Baroreceptors fire at a higher rate.

  • Triggered Response:

    • Initiates parasympathetic stimulation of the heart.

    • Decreases sympathetic stimulation of peripheral arterioles (leading to vasodilation).

    • Results in a decrease in cardiac output.

Function During Hypotension

  • Baroreceptors fire at a lower rate.

  • Triggered Response:

    • Initiates sympathetic stimulation of the heart.

    • Increases sympathetic stimulation of peripheral vessels (leading to vasoconstriction).

    • Results in an increase in cardiac output.

Chemoreceptors

  • Definition: Sensitive to levels of O2, CO2, and H+; located in close proximity to baroreceptors.

  • Function:

    • Respond to an increased level of CO2 and decreased levels of H+ by stimulating cardioaccelerator and vasomotor centres, resulting in increased cardiac output.

    • Effects:

    • Increased HR and force of contraction.

    • Increased vascular tone (vasoconstriction).

  • Respond to decreased CO2 and increased H+ by stimulating cardioinhibitor centres and suppressing vasomotor centres, resulting in decreased cardiac output.

    • Decreased HR and force of contraction.

    • Decreased vascular tone (vasodilation).

Endocrine Control

  • The endocrine system influences cardiovascular homeostasis through two main mechanisms:

    1. Release of catecholamines:

    • Epinephrine

    • Norepinephrine

    1. Hormones interacting with the kidneys, which regulate blood volume.

Catecholamines

  • Definition: Epinephrine and norepinephrine are released by the adrenal medulla.

  • Effects:

    • Enhance and extend the sympathetic response:

    • Increased heart rate

    • Increased force of contraction

    • Causes vasoconstriction to organs that are deemed "nonessential" during fight-or-flight response.

    • Redirects blood perfusion to the liver, muscles, and heart.

Hormones: Antidiuretic Hormone (ADH)

  • Source: Secreted by cells in the hypothalamus and transported to the posterior pituitary.

  • Release Trigger: Stimulated by increased osmolality (low water content in the blood).

  • Mechanism:

    • Binds to receptors on collecting ducts and distal tubules of the kidneys (where urine is formed).

    • Causes water to move from the kidney tubules back into the blood, resulting in less water being excreted in urine and restoring blood volume and pressure.

    • Stimulates peripheral vasoconstriction.

Secretion Triggers for ADH

  • Increased osmolality (due to dehydration).

  • Decreased plasma volume.

  • Cholecystokinin (CCK) from the small intestine.

  • Increased levels of Angiotensin II (Ang II) activates secretion from the posterior pituitary.

Hormones: Renin-Angiotensin-Aldosterone Mechanism

  • Renin:

    • An enzyme that converts angiotensinogen (produced by the liver) to angiotensin I.

  • Conversion Process:

    • Angiotensin I is converted to angiotensin II in the lungs by Angiotensin Converting Enzyme (ACE).

  • Angiotensin II:

    • A powerful vasoconstrictor that stimulates:

    • ADH release, which increases blood volume.

    • Aldosterone release, which increases sodium reabsorption in the kidneys.

    • Water follows sodium, thereby increasing blood volume.

Renin-Angiotensin System Process

  • In the event of a drop in blood pressure or fluid volume:

    • The liver releases angiotensinogen.

    • Renin is released from the kidney and converts angiotensinogen to angiotensin I.

    • ACE converts angiotensin I to angiotensin II.

    • Angiotensin II acts directly on blood vessels to stimulate vasoconstriction.

    • Angiotensin II stimulates the adrenal gland to release aldosterone, leading to the reabsorption of sodium and water from the kidneys.

Hormones: Erythropoietin (EPO)

  • Source: Released by kidneys in response to low blood flow and low O2 concentrations.

  • Function: Stimulates the production of erythrocytes in the bone marrow, increasing blood viscosity.

  • Less immediate factor for blood volume but has a role in vasoconstriction.

Hormones: Atrial Natriuretic Hormone (ANP)

  • Source: Secreted by cells in the atrial wall when blood volume is sufficiently high to overstretch cardiac cells.

  • Function: Antagonist to angiotensin II.

    • Promotes sodium loss (thereby water loss) from the kidneys.

    • Suppresses production and release of renin, aldosterone, and ADH.

    • Results in fluid loss, thereby decreasing blood volume and pressure.

Summary

  • Neural, endocrine, and autoregulatory mechanisms significantly affect:

    • Blood flow

    • Blood pressure

    • Perfusion of blood to body tissues.

  • Neural mechanisms include:

    • Cardiovascular centres in the medulla oblongata.

    • Baroreceptors located in the aorta, carotid arteries, and right atrium.

    • Associated chemoreceptors monitoring blood levels of O2 and CO2.

  • Endocrine controls include:

    • Epinephrine and norepinephrine.

    • ADH, renin-angiotensin-aldosterone mechanism, ANP, and EPO.

  • Autoregulation refers to local control of vasodilation and constriction via chemical signals and the myogenic response.