Cardiovascular Control Mechanisms

• There are three levels of control of blood pressure and blood flow
  • Neural Control
  • Hormonal Control
  • Local Control

Mechanisms of Homeostasis

• Receptors sense changes in the internal or external environment
• The control center processes information gathered from receptors and sends a response to the effectors
• The effector adjusts the regulated parameter

Feedback Loops

• Negative feedback loops cause the control mechanism to counteract further changes of the parameter in the same direction
• Positive feedback loops amplify changes of the parameter in the same direction

Neural Control: The Cardiovascular (CV) Center

• Located in the medulla oblongata
• Includes a collection of gray matter regions (nuclei)
• 2 cardiac centers
• The vasomotor center
• Helps regulate HR, SV, and blood vessel diameter
• Receives input from higher brain centers including the cerebral cortex, the limbic system, and the hypothalamus
• Also receives input from peripheral afferent nerve fibers, including baroreceptors, chemoreceptors, and proprioceptors

CV Center Input

• Increased frequency of sensory nerve impulses
• Input from higher brain centers - cerebral cortex, limbic system, and hypothalamus
• Input from proprioceptors monitoring joint movements
• Input from baroreceptors monitoring blood pressure
• Input from chemoreceptors monitoring blood acidity (H+), CO2, and O2

CV Center Output

• Increased frequency of motor nerve impulses
• Heart rate decreases
• Heart rate and contractility increase
• Blood vessels undergo vasoconstriction

Nuclei of the CV Center

• The CV center is composed of three major functional regions:
  • Cardioacceleratory Center: sympathetic neurons, increase HR and contractility
  • Cardioinhibitory Center: parasympathetic neurons, decrease heart rate
  • Vasomotor Center: "vasomotor neurons", regulate blood vessel diameter via sympathetic nerves, arteriolar smooth muscle, and cause vasoconstriction
• Cardiovascular reflexes are produced by afferent signaling of:
  • Baroreceptors
  • Chemoreceptors
  • Proprioceptors
• Baroreceptors are the most important receptors in CV regulation

Chemoreceptors

• Located in the carotid sinus and in the walls of the ascending aorta
• In the carotid sinus, signals the medulla via cranial nerve IX
• In the aortic bodies, signals the medulla via cranial nerve X
• Chemoreceptors respond to increased hydrogen ion content, and increased CO2
• Chemoreceptors respond most strongly to hypoxia
• Chemoreceptors activate the sympathetic division, leading to increased HR, SV, and vasoconstriction

Baroreceptors

• High-pressure baroreceptors are in the carotid sinus and aortic arch
  • Enter the CV center via cranial nerves IX & X
• Low-pressure baroreceptors are located in the walls of the right atrium and vena cavae
  • They enter the CV center via cranial nerve X

Baroreceptor-Initiated Reflex in Response to Decreasing Blood Pressure

• Decreasing blood pressure disrupts homeostasis
• Baroreceptors in the arch of the aorta and carotid sinus are stretched less
  • Decreased rate of nerve impulses
• The CV center in the medulla oblongata and adrenal medulla act as control centers
  • Increased sympathetic, decreased parasympathetic stimulation
  • Increased secretion of epinephrine and norepinephrine from the adrenal medulla
• Effectors:
  • Stroke volume and HR increase (increased cardiac output)
  • Blood vessels constrict (increased systemic vascular resistance)
• Return to homeostasis when increased cardiac output and increased vascular resistance brings blood pressure back to normal

Baroreceptor-Initiated Reflex to Elevated Blood Pressure

• Arteries stretch
• Baroreceptors increase firing rate
• Cardioinhibitory neurons stimulate
• Vasomotor center is inhibited
• Reduced heart rate and vasodilation leads to reduced sympathetic tone and vasomotor tone

Hormonal Control of Blood Pressure

• Catecholamines (Epinephrine & NE):
  • Cause arteriole & vein vasoconstriction
  • Increase HR & SV
• Antidiuretic hormone (ADH):
  • Causes intense vasoconstriction
  • Decreases water loss in cases of extremely low blood pressure
• Angiotensin II:
  • Causes intense vasoconstriction when renal perfusion is inadequate (BP is too low)
• Aldosterone:
  • Causes water retention
  • Increases blood volume when blood pressure is too low
• Atrial natriuretic peptide:
  • Causes vasodilation and water loss when blood pressure is too high
• Histamine:
  • Causes vasodilation
  • Increases blood flow

Catecholamines

• Catecholamines (NE and Epinephrine) circulate and bind directly to cardiac muscle fibers and blood vessel smooth muscle cells
• Effect is an increase in HR and SV, and constriction of veins and arterioles
• Arteries supplying the brain and heart have little smooth muscle; they are not subject to vasoconstriction by the sympathetic division or catecholamines
  • These vessels autoregulate

Anti-diuretic hormone (ADH)

• Produced by the hypothalamus and released from the posterior pituitary when blood loss is severe, and blood pressure is reduced
• Causes widespread vasoconstriction
• Causes decreased water loss from skin & urine

Angiotensin II

• One of the most powerful vasoconstrictor substances known
• Acts on all arterioles simultaneously when released into the blood
• Results in an increase in vascular resistance (when blood pressure is too low)

RAA System Cascade

• Low blood pressure causes the release of renin by the kidney;
  • Angiotensinogen (released by the liver) converts renin into angiotensin I
  • The lungs convert AT I into AT II by angiotensin converting enzyme (ACE), located in the endothelial cells of the lung

Aldosterone

• Angiotensin controls aldosterone secretion
• When AT II levels increase, aldosterone is secreted by the adrenal cortex
• Aldosterone increases salt and water reabsorption
  • Raises blood volume which raises blood pressure
• Powerfully stimulates the thirst center

Atrial natriuretic peptide & Histamine

• ANP is released by cells of the atria when blood pressure is high
  • Causes vasodilation and promotes loss of water and salt by the kidneys
  • Collectively reduces blood volume and vasoconstriction
• Histamine is released by mast cells
  • Causes vasodilation by relaxing blood vessel smooth muscle
  • especially important in increasing the rate of blood flow to inflamed or damaged tissue

Local Control of Blood Pressure

• Neural regulation of flow refers to changes in flow due to vasoconstriction
• Humoral flow control refers to changes in vessel diameter due to circulating hormones
• The major regulatory factor is tissue metabolic activity
• Metabolic, or "local" regulation, is blood vessel dilation due to substances released by tissue cells

Integrated Responses to Low Blood Pressure

• Hypovolemic shock disrupts homeostasis
• Blood volume and blood pressure moderately decrease
• Increased secretion of renin
• Baroreceptors detect these disruptions
  • Located in juxtaglomerular cells in the kidneys
  • Located the aorta and carotid sinus
• CV center in medulla oblongata acts as a control center
  • Triggers increased sympathetic stimulation/hormones from adrenal medulla
• The hypothalamus & posterior pituitary act a control center
  • Triggers the release of ADH
• Effector responses bring blood volume and pressure back to normal
  • Increased sympathetic stimulation to the heart to raise HR and contractility, and cause vasoconstriction of blood vessels
  • Kidney stimulation leading to conservation of salt and water
  • Increased levels of aldosterone