Control of blood pressure Flashcards
What is the baroreceptor reflex? Why is it important?
A speedy negative feedback response to a detected change in MAP. It reduces the minute-by-minute change in MAP
Where are the sensory receptors for the baroreceptor reflex located? What do they detect? Which is more important? Why?
High-pressure baroreceptors In the aortic arch and the carotid sinus (bifurcation of the carotid artery). Detect stretch in vessel walls. Carotid sinus is more important b/c it’s more sensitive
What are the afferent pathways in the baroreceptor reflex? Efferent pathways?
Afferent- From aortic arch- Cr. X
From carotid sinus- Hering’s nerve to Cr. IX
Efferent- autonomic NS (symps and paras)
What is the central integrating center for this reflex? Where is it located in the brain? What goes on here?
The nucleus tractus solitarius (NTS) in the medulla. It compares the signals from the receptors to its set point for MAP and orchestrates the ANS response
What are chemoreceptors? Where are they located and when are they important?
Receptors that detect partial pressures of O2 and CO2 and blood pH. Peripheral ones are in the carotid sinus and aortic arch. Central ones are in the medulla. They help control arterial pressure when it falls below 80 mm Hg
When a baroreceptor is stretched, what happens? How does this change with more or less stretch?
An increase in transmural pressure stretches the receptors, causing more depolarization in the sensory nerves (large initial depolarization followed by a more modest, steady depolarization). Greater stretch= greater depolarization (both initially and at the plateau) causing more firing of the nerve.
What is the range of baroreceptors? Where are they most sensitive? Why is this important?
About 50-60 mm Hg to 180 mm Hg. Most sensitive around 100 mm Hg (normal MAP) so small changes in pressure cause strong feedback changes.
How does the baroreceptor reflex change with a long term change in arterial pressure (i.e. hypertension)?
The set point in the NTS changes and the BP v. # nerve impulses curve shifts (to the R in the case of hypertension since MAP is higher now)
What is the valsalva maneuver? What effect does it have on HR?
Expiration against a closed glottis increases thoracic pressure, decreasing venous return to the heart (and thus CO and MAP). If your baroreceptor reflex is working, your NTS will signal an increase in SNS output to raise MAP and your HR will increase.
What is carotid sinus massage? What effect does it have on heart rate?
It stimulates the baroreceptors in the carotid sinus, slowing HR (used to treat atrial tachycardia sometimes)
If MAP is increased, what will the NTS do in response?
Increase PNS stim to decrease HR
Decrease SNS stim to decrease HR and SV (via decreased ventricle tone and decreased venous return) thus decrease CO. Decreased SNS output also lowers peripheral R (b/c decreased arterial tone) and all of this combines to lower MAP to restore it to the normal value.
If MAP is decreased, what will the NTS do in response?
Decrease PNS and increase SNS output- increase HR
Increased SNS also means increased R in arterioles, increased venous tone (and increased EDV), increased ventricular contractility (increased SV). CO increases and so does MAP
An detected increase in MAP corresponds to a/an (increase/decrease) in action potential firing to the NTS. A decrease in MAP corresponds to a/an (increase/decrease) in firing.
Increased MAP- increased firing
Decreased MAP- decreased firing.
The NTS is always receiving signals from the baroreceptors
What is the overall response to a perceived increase in MAP? A perceived decrease?
Perceived increase- to decrease MAP, the NTS orchestrates bradycardia and vasodilation
Perceived decrease- tachycardia and vasoconstriction to increase MAP
How does an increase in arterial tone increase EDV?
Increased arterial tone means R arteriole increases which means capillary pressure moves closer to venous pressure so more blood is reabsorbed, increasing blood volume and thus EDV
How can the body rapidly regulate MAP? How about over an intermediate time scale? Or long term?
Rapid- Baroreceptors (high and low pressure), chemoreceptors, CNS ischemic response
Intermediate- Renin-angiotensin vasoconstriction, fluid shifts, ADH/vasopressin
Long term- renin-angiotensin retention, aldosterone release, thirst
When is the CNS ischemic response activated? How is it activated? What does it stimulate?
Activated when MAP is below 60 mm Hg and especially active when it falls to 15-20 mm Hg. It responds to increased CO2/decreased pH in the blood, causing lots of peripheral vasoconstriction and the kidneys to stop producing urine
What sets off the Cushing reaction? How does it work?
Increased pressure of the CSF that cuts off blood supply to the brain. This reaction causes arterial pressure to rise above CSF pressure so that the vital centers of the brain still receive blood
What do low-pressure baroreceptors respond to? What do they stimulate? Where are they located?
Respond to decreased volume (with a decreased firing rate) causing vasoconstriction and ADH release. Located in atria and pulmonary vessels
What must happen to produce angiotensin II?
MAP must decrease, SNS must stimulate the kidneys to produce renin which cleaves angiotensinogen to produce angiotensin I. This must travel to the lungs where it’s cleaved by ACE (angiotensin converting enzyme) into angiotensin II, the active form.
What effects does angiotensin II have on the body?
It causes vasoconstriction, renal retention of salt and water and aldosterone release
What is the “fluid shift”? Why does this occur?
Decreased blood volume causes decreased capillary hydrostatic pressure which drives fluid absorption into the blood and increases blood volume
What stimulates ADH release?
Increased body fluid osmolality; decreased blood volume; decreased blood pressure; angII; pain; stress; nausea/vomiting
What inhibits ADH release?
Decreased body fluid osmolality; increased blood volume; increased blood pressure; ANP; ethanol
Where is ADH synthesized? Where is it stored? What does it do?
Synthesized in the hypothalamus and stored in the posterior pituitary. Acts on the kidney to promote sodium and water retention. Also promotes vasoconstriction
Name some of the endogenous vasoconstrictors. Name some vasodilators.
Vasoconstrictors- AngII, ADH, endothelin
Vasodilation- ANP, NO, (adenosine, histamine)
What are the three phases of circulatory shock? At which stage can you no longer recover?
Compensated, progressive and end stage. At end stage.
You hemorrhage. What does your body do in response?
The decrease in MAP sets off your high-pressure baroreceptors which try to increase your CO by increasing your HR, contractility, and VR. They also increase TPR. Ang II and ADH increase your TPR as well; they + aldosterone, fluid shifts, and thirst increase your blood volume. All of these things combine to raise your MAP back towards normal.
Of all these mechanisms, which has the greatest gain?
The renal blood pressure-volume control mechanisms (i.e. renin-angiotensin-aldosterone)
