20.6 Regulation of Blood Pressure and Blood Flow

Blood pressure is dependent upon 3 primary variables

• cardiac output

• resistance

• blood volume

Short-term nervous system regulation of blood pressure occurs

through autonomic reflexes involving nuclei within the medulla oblongata of the brainstem.

Autonomic reflexes

control blood pressure and are homeostatic systems that are regulated by negative feedback loops.

involves the 5 components of a reflex arc.

The components of the autonomic reflexes regulating blood pressure

• baroreceptors

• sensory neurons

• cardiovascular center (control center)

• motor neurons of the ANS

• the heart and blood vessels (the effectors)

Sensory receptors

detect stimuli and relay sensory input to the central nervous system.

The most significant types of sensory receptors in regulating blood pressure

baroreceptors

Baroreceptors

specialized sensory nerve endings in blood vessel walls that respond to stretch

they detect changes in stretch of the blood vessel wall when the blood volume within the blood vessel changes (decreases or increases)

2 primary locations of baroreceptors within the cardiovascular system

• aortic arch

• carotid sinuses, specifically within the tunica externa

The baroreceptors in the aortic arch

monitor change in stretch of the aorta and in response alter signals that are relayed along sensory neurons(within the vagus nerve) to the cardiovascular center

The baroreceptors in the aortic arch are important in

monitoring systemic blood pressure.

Carotid sinus

the baroreceptors located within a slightly enlarged region of each internal carotid artery.

the baroreceptors in the carotid sinuses monitor

change in stretch of the internal carotid arteries, which transport blood to the brain. In response, these baroreceptors alter signals that are relayed along sensory neurons (within the glossopharyngeal nerve) to the cardiovascular center.

they also monitor blood pressure changes in the head and neck

The baroreceptors in the carotid sinuses are important in

monitoring blood pressure affecting the brain.

Baroreceptors in the carotid sinuses are more sensitive to

blood pressure changes since it is given the importance of delivering sufficient blood to the brain.

2 distinct groups of nuclei within the medulla oblongata that participate in the regulation of blood pressure, specifically the cardiac center and vasomotor center, which is called

cardiovascular center

the cardiac center regulates

heart activity and cardiac output

the vasomotor center controls

the degree of vasoconstriction and vasodilation of blood vessels and regulates resistance

Motor neurons of the sympathetic division extend

from the cardioacceleratory center to both the

• Sinuatrial(SA) node

• atrioventricular(AV) node

Nerve signals from the SA and AV nodes causes release of

• norepinephrine from their ganglionic neuron

which then

• increases the firing rate of the SA node

• shorten the delay of signals at the AV node as they are relayed along the heart’s conduction pathway.

sympathetic stimulation increases

heart rate.

Sympathetic division pathways extend to the myocardium; when stimulated

cause a forceful contraction of the heart and increases stroke volume. which then produces a larger cardiac output.

Motor neurons of the parasympathetic division extend from

the cardioinhibitory center to also innervate both the SA node and AV node.

Nerve signals relayed along these parasympathetic pathways (including motor neurons within the vagus nerve) causes

• the release of acetylcholine from their ganglionic neurons

which both

• decreases the firing rate of the SA node and

• lengthens the delay of signals at the AV node as they are relayed along the heart’s conduction pathway

parasympathetic stimulation decreases

heart rate and produces a smaller cardiac output.

Vasomotor center regulates

blood vessels, both the degree of vasoconstriction and vasodilation.

blood vessels do not have

dual innervation.

they are typically innervated by only the sympathetic division with no innervation by the parasympathetic division.

Only sympathetic division pathway extends from the vasomotor center to most blood vessels…

• norepinephrine is released from these ganglionic neurons

Variations in response of blood vessels (vasoconstriction and vasodilation) is dependent upon

the subtypes of receptors in the smooth muscle cells within the tunica media of the blood vessel wall.

The receptor subtype is specific to the location of the blood vessels within the different vascularized tissues of the body (skeletal muscle, skin)

The smooth muscle cells typically contain 1 of several receptor subtypes that bind

different neurotransmitters and hormones

2 of the most common subtypes

• alpha

• beta receptors

Smooth muscle cells that contain alpha receptors

contract in response to norepinephrine which causes vasoconstriction of these blood vessels (most blood vessels in the body)

Smooth muscle cells that contain beta receptors

relax in response to epinephrine hormone, which causes vasodilation of these blood vessels (coronary arteries, arteries supplying skeletal muscle)

Activation of the sympathetic division of the ANS and subsequent stimulation of the adrenal medulla cause the following:

• increased peripheral resistance: More blood vessels are stimulated to vasoconstrict than vasodilator because there are more blood vessels that house smooth muscles with alpha receptors than beta receptors; consequently, peripheral resistance is increased, raising blood pressure

• Larger circulating blood volume: Vasoconstriction of veins shifts blood from venous reservoirs and circulating blood volume increases, thus increasing blood pressure

• Redistribution of blood flow: More blood flow reaches skeletal muscle and the heart, and less blood flow goes to most other structures. Thus, organs requiring additional nutrients and oxygen have adequate perfusion.

If blood pressure decreases:

• Sensory receptor. Decreased stretch in the blood vessel wall (reflecting a decrease in blood pressure, as might occur when you arise from bed in the morning) is detected by baroreceptors in the aortic arch, carotid sinuses, or both.

• Sensory neurons. The baroreceptors decrease the frequency of signals relayed along sensory neurons within the vagus and glossopharyngeal nerves to both the cardiac center and vasomotor center composing the cardiovascular
  center.

• Control center. The cardiovascular center alters nerves signals initiated and then relayed along autonomic motor neurons.

• Motor neurons. Altered frequency of signals are relayed along both sympathetic and parasympathetic motor neurons.

• Effectors. The SA node, AV node, and myocardium of the heart, as well as blood vessels, are induced to change.

A decrease in blood pressure leads to the following changes in the cardiac center

• the cardioacceleratory center increases signals relayed along sympathetic pathways extending to the heart, including the SA node, AV node, and the myocardium.

• the cardioinhibitory center decreases signals relayed along parasympathetic pathways that extend to the SA node and AV node.

• As a result, both heart rate and stroke volume increase which results in a larger cardiac output.

A decrease in blood pressure leads to the following changes in the vasomotor center

• increases signals along sympathetic pathways to blood vessels, resulting in net vasoconstriction, resulting in increased resistance, along with shifting of blood from venous reservoirs. consequently, blood flow increases.

• the resulting increase in cardiac output, increase in resistance, and larger circulating blood volume quickly elevate blood pressure to maintain sufficient blood pressure to move blood through the vasculature.

If blood pressure increases:

• Sensory receptor. Increased stretch in the blood vessel wall (reflecting an increase in blood pressure) is detected by baroreceptors in the aortic arch, carotid sinuses, or both.

• Sensory neurons. The baroreceptors increase the frequency of signals relayed along sensory neurons within the vagus nerve (CN X) and glossopharyngeal nerve (CN IX) to both the cardiac center and vasomotor center composing the cardiovascular center.

• Control center. The cardiovascular center integrates and processes incoming sensory input and alters signals relayed along motor neurons.

• Motor neurons. Altered frequency of signals are relayed along both sympathetic and parasympathetic motor neurons.

• Effectors. The SA node, AV node, and myocardium of the heart, as well as blood, vessels are induced to change.

A increase in blood pressure leads to the following changes in the cardiac center

• decreases signals relayed along sympathetic pathways extending to the heart, including the SA node, AV node, and myocardium

• the cardioinhibitory center increases signals relayed along parasympathetic pathways that extend to the SA node and AV node.

• Both heart rate and stroke volume decrease, resulting in smaller cardiac output.

A increase in blood pressure leads to the following changes in the vasomotor center

• decreases signals along sympathetic pathways to blood vessels, resulting in net vasodilation, resulting in decreased resistance, along with shifting of blood to venous reservoirs. consequently blood flow decreases

• The resulting decrease in cardiac output, decrease in resistance, and smaller circulating blood volume lower blood pressure, and blood flow returns to its resting levels.

Baroreptors respond best to

sudden, short-term changes in blood pressure.

Chemoreceptors are most important in

regulating respiration.

chemoreceptors are secondarily involved in

regulating blood pressure.

When chemoreceptors are stimulated,

they inititate chemoreceptor reflexes,

chemoreceptor reflexes

negative feedback loops that ultimately bring blood chemistry levels back to pre-stimulus levels.

2 main peripheral chemoreceptors

• aortic bodies

• carotid bodies.

aortic bodies are located

in the aortic arch

carotid bodies are located

at the bifurcation of each common carotid as it splits into an external carotid and an internal carotid artery.

Both aortic and carotid bodies

send sensory input to the cardiovascular center

aortic bodies send signals via the vagus nerve

the carotid body send signals along the glossopharyngeal nerve.

High carbon dioxide levels, low pH, and very low oxygen levels stimulate the

chemoreceptors, and the resulting increase in signals relayed along sensory neurons primarily stimulate the vasomotor center.

The vasomotor center responds by increasing signals along sympathetic neurons to blood vessels, which increases resistance and shifts blood from venous reservoirs to increase venous return.

the changes raise blood pressure and increase blood flow, including blood flow to the lungs, which allows for an accompanying change in respiratory gas exchange.

As a result, blood gas levels return to pre stimulus levels.

Blood pressure is also influenced by

higher brain centers.

Several hormones in addition to epinephrine and norepinephrine released from the adrenal medulla, participate in

regulating blood pressure by altering resistance, and blood volume or both.

fluid output occurs through

• expired air,

• sweat

• transpiration

• feces

• urine.

urine volume increases,

blood volume decreases.

decreasing urine output

helps to maintain blood volume by decreasing loss of blood plasma that is filtered at the kidneys.

4 primary hormones regulating blood pressure

• angiotensin II

• antidiuretic hormone

• aldoserone

• atrial natriuretic peptide.

The Renin-angiotensin system (in relation to blood pressure)

"straddles" short-term neural regulation and long-term hormonal regulation of blood pressure because the synthesis of the angiotensin II is initiated by the nervous system (short-term mechanisms), and angiotensin II causes the release of other hormones (long-term mechanisms).

angiotensinogen

plasma protein, produced by the liver which is continuously released into the blood.

The kidney releases the enzyme renin into the blood in response to either

• low blood pressure

• stimulation by the sympathetic division

within the blood, renin converts angiotensinogen into

angiotensin I.

Angiotensin I is then converted to

angiotensin II by angiotensin-converting enzyme (ACE)

angiotensin-converting enzyme (ACE)

an enzyme associated with capillary endothelium. ACE is found in very high concentrations on the pulmonary capillary endothelium. so most (but not all) angiotensin I conversion to angiotensin II occurs within the blood vessels of the lungs.

Having most of the ACE in the pulmonary capillary endothelium helps ensure

that sufficient angiotensin I is converted to angiotensin II. This is because all blood moves through the pulmonary circulation to be oxygenated, so contract between angiotensin I and ACE is maximized.

In general, Ang II alters blood pressure by influencing

• Blood vessels. Angiotensin II is a powerful vasoconstrictor of blood vessels-much more powerful than comparable hormones, such as norepinephrine-and thus it increases peripheral resistance and raises blood pressure to a greater extent. (You can remember this specific action for angiotensin II by
  remembering that angos = vessel and tensin = tension, which is what
  angiotensin II induces in the blood vessel by stimulating vasoconstriction.)

• Blood volume: Increasing fluid intake. Ang II also potentially increases blood volume because it stimulates the thirst center within the hypothalamus (see L section 13.4c); fluid intake (if it occurs) increases blood volume, which increases blood pressure.

• Blood volume: Decreasing urine output. Ang II acts on the kidneys directly to decrease urine output (see ' section 24.5e and L section 25.4a). Ang Il also stimulates the release of other hormones and has indirect effects on the kidney through these hormones. Ang II stimulates the release of (a) antidiuretic hormone (ADH) from the posterior pituitary via the hypothalamus (see L section 17.7b) and (b) aldosterone from the adrenal cortex (see L section 17.9a). These two hormones (ADH and aldosterone) also act on the kidneys to decrease urine formation, which helps to maintain blood volume, and thus blood pressure.

Antidiuretic hormone (ADH)/vasopressin

released from the posterior pituitary in response to nerve signals from the hypothalamus.

alters blood pressure in ways similar to and II, but its primary effect is through the kidney.

• Blood volume: Decreasing urine output. ADH, like Ang II, acts on the kidneys to decrease urine formation, which helps to maintain blood volume and thus blood pressure (see L section 24.6d and L section 25.4b). (You can remember this specific action for antidiuretic hormone by remembering that
  anti = against and ouresis = urination, which is what ADH induces in the
  kidney-"anti-urination.")

• Blood volume: Increasing fluid intake. ADH also potentially increases blood volume because, like Ang II, it stimulates the thirst center within the hypothalamus (see L' section 13.4c); fluid intake (if it occurs) increases blood volume, which increases blood pressure.

• Blood vessels. ADH, like Ang II, is a vasoconstrictor-but only in high doses.
  Thus, like Ang II, it can increase peripheral resistance and raise blood pressure. This effect as a vasoconstrictor is the reason ADH is also referred to vasopressin.

Aldosterone

functions through the kidney, by stimulating increased absorption of sodium ion (Na+) and water. This decreases their loss in the urine and helps maintain blood volume and blood pressure.

Atrial natriuretic peptide(ANP)

released from the atrium of the heart in response to an increase in stretch of the atrial walls due to increased blood volume and increased venous return.

• stimulates vasodilation, which decreases peripheral resistance

• increases urine output, which decreases blood volume

• the net effect is decrease in blood pressure