Lec. 10. ABP regulation cont.

Intro.

ABP regulation mechanisms can be classified into immediate, intermediate, and long-term regulation mechanisms.

Short-term immediate control mechanisms.

Always nervous mechanisms, and occur within seconds.

Arterial baroreceptors (pressure receptors.)⭐

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In the wall of carotid sinus and aortic arch (and large arteries) sending their signals through the glossopharyngeal and vagus nerves. They respond to pressure changes of the blood (type A baroreceptors.)

Mechanism:

• Always send depressor impulses (if they sense increased ABP) to cardioaccelerator center (decreased HR $\to$ decreased COP $\to$ decreased ABP), vasoconstrictor center (VD $\to$ decreased TPR $\to$ decreased ABP), respiratory center (decreased respiratory rate $\to$ decreased HR $\to$ decreased COP $\to$ decreased ABP), and adrenaline secretory center (decreased NE and EN secretion.)
• The depressor impulses can be reduced (but are still depressor, not pressor impulses) to increase ABP if it is too low (increased HR, VC, etc…)

Characters:

• Rapid response to ABP.
• Negative feedback control system.
• Activated from 50 - 180 mmHg (impulse rate increases the more you increase ABP above 50, reaching a maximum rate at 180 mmHg.)
• Slowly adapting, 1 - 2 days of consistent ABP change causes baroreceptors to adapt to maintain new ABP (resetting of baroreceptor reflex.)

Peripheral chemoreceptors.⭐

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In the carotid and aortic bodies (a collection of cells near the carotid sinus and aorta) they sense $\downarrow O_2$ , $\uparrow C{O}_2$ , and $\uparrow H^{+}$ concentrations that are synonymous with hypoxia of tissue. They send their signals through the glossopharyngeal and vagus nerves and only activate when ABP < 60 mmHg.

Mechanism:

• Sensing $\downarrow O_2$ , $\uparrow C{O}_2$ , and $\uparrow H^{+}$ concentrations caused by decreased BF (a sign of low ABP) and sending pressor impulses to cardioaccelerator center (increasing HR $\to$ etc…), vasoconstrictor center (VC $\to$ etc…), and adrenaline secretory center (increased NE and EN secretion.)

(Denervation of the receptors can change the ABP according to the state of ABP at the time of denervation. Low ABP will be lower after denervation, high ABP will be higher after denervation.)

Atrial baroreceptors (volume receptors.)⭐

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Found inside the walls of both atria, and play an important role to minimize ABP change as a result of changes in blood volume. They respond to volume changes of the blood (type B baroreceptors.)

Mechanism:

Sensing increased BV (through sensing the stretch in atrial walls due to increased VR), the atrial baroreceptors cause:

• VD of veins $\to$ decreased venous return & arterial BV (blood is shunted to the venous side.)
• VD of arterioles $\to$ decreased TPR $\to$ decreased ABP.
• VD of renal arterioles $\to$ increased GFR $\to$ increased fluid loss through urination $\to$ decreases BV to normal.
• Impulses to hypothalamus $\to$ decreased ADH secretion $\to$ decreased water reabsorption $\to$ increased fluid loss through urination $\to$ decreases BV to normal.

CNS ischemic response.⭐

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It is a very powerful response to ischemia in the CNS (the ischemia being caused by bleeding for example), especially the brain. Its a last ditch effort to try to maintain blood flow to the brain.

Mechanism:

This response only works when ABP is below 60 mmHg, reaching maximum activation at 20 mmHg, this dangerously low BP causes decreased BF to the brain, initiating the response:

• Decreased ABP $\to$ decreased cerebral BF $\to$ cerebral ischemia $\to$ strong vasomotor center stimulation $\to$ peripheral VC and tachycardia $\to$ increased ABP $\to$ increased BF to the brain. In cases where increased cranial pressure is the cause of cerebral ischemia, Cushing’s reaction occurs which causes the same effects as CNS ischemic responses but with bradycardia instead (due to pressure on the brainstem causing depression of the cardiac centers.)

Intermediate control mechanisms.

Occur within a few minutes.

Renin-angiotensin aldosterone system.⭐

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Activates in response to decreased renal blood flow.

Mechanism.

• Decreased ABP $\to$ decreased renal BF $\to$ juxtaglomerular cells secrete renin $\to$ renin activates angiotensinogen (inactive angiotensin) to angiotensin 1 $\to$ angiotensin 1 is converted to angiotensin 2 in lung. Angiotensin 2 causes:
• Potent vasoconstriction.
• Increases secretion of ADH causing no urine production and increased water.
• Increases secretion of aldosterone causing increased Na retention. Ultimately, it causes an increase in ABP.