baroreceptor/chemoreceptor reflexes

[Aclamity]

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I'm trying to make sense of these but they keep on getting boggled in my mind.

When the baroreceptors in the aortic arch/carotid bodies sense changes in BP do they only modify HR and contractility, or do they also inc/dec respiration?

What about the chemoreceptors in the brain? When they sense inc PCO2 I know they cause increased respiration, but do they also cause inc HR/contractility (to get more blood flow to the brain)?

Finally, I know FA says that central chemoreceptors dont' respond to dec O2 (until about 50 mmHg), but when they do what is their response? I would think it would increase respiration, but when I read about the Cushing reflex it sounded like it caused inc HR/contractility (like a baroreceptor reflex)

Thanks!

 

[Morsetlis]

The baroceptors that sense a change in BP modify para/sympathetic activity. Specifically, increased vagal tone (increasing BP) will shift the balance toward parasympathetic activity.

The chemoceptors in the brain sense diffused CO2 that form carbonic acid (H+). They only deal with ventilation.

The peripheral chemoceptors sense O2 and H+. They also deal with ventilation. Specifically, these are glomus cells.

The Cushing's Reflex sense changes in BP, not C/O2. There are apparently also baroceptors in the brain which complement yet have opposite actions on baroceptors in the carotid bodies/aoarch.

Physical distortion of the vagus nerve and brain stem due to increased ICP will lead to bradycardia and slowed respiration.

 

[AndyRSC]

The Cushing's Reflex sense changes in BP, not C/O2. There are apparently also baroceptors in the brain which complement yet have opposite actions on baroceptors in the carotid bodies/aoarch.

Where are you getting that from? Of course it has to do with CO2. It's ischemia-driven.

 

[Aclamity]

Where are you getting that from? Of course it has to do with CO2. It's ischemia-driven.

This is probably what ended up confusing me the most. Assuming it's CO2-driven (which I thought it was), and assuming the central chemoreceptors deal ONLY with ventilation, shouldn't the ischemia simply lead to an increase in ventilation?

However, according to what I've read on the Cushing Reflex, the ischemia ends up causing an increase in HR/contractility/BP (which then goes on to overstimulate the carotid baroreceptors, leading to bradycardia, etc etc).

But the point is, the cushing reflex kinda conflicted with what I was taught (that the central chemoreceptors only affect ventilation). My only explanation for this was that the decrease in O2--not the increase in CO2--is what was driving the cushing reflex and causing inc BP. But then again, that's just me trying to BS my way into a logical explanation. I'd really love to know the ACTUAL answer haha

 

[Morsetlis]

Where are you getting that from? Of course it has to do with CO2. It's ischemia-driven.

The mechanism is not clear. It's ischemia-driven, yes, but there are no "oh this cell does this with this Gs protein".

Guyton:

Considering that the ischemic response has a PRESSURE-threshold, I would say that it's pressure-driven.

 

[AndyRSC]

Hah, I loved Guyton, but according to that book NOTHING is known for sure, even the most basic physiologic processes every source confidently states as fact.

Considering that the ischemic response has a PRESSURE-threshold, I would say that it's pressure-driven.

Not sure how you're still coming up with that, especially after what you just posted. It says "this initiates an ischemic reaction." Of course the reaction has a pressure threshold; pressure has to be kept above ICP in order for perfusion to take place, just like any other part of the body. If there's no perfusion, cerebral PCO2 builds up, and a vasomotor response is activated. Both Guyton (in the section right before the one you posted) and Constanzo are clear about this.