Chemoreceptors in BP control

[Sir Gillies]

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Am I correct in saying that BP is mainly controlled by baroreceptors. But chemoreceptors also may play role and if not influenced by respiratory modulation, then hypoxia (or hypercapnia/acidosis) causes:
- Decrease firing of peripheral chemoreceptors
- decrease afferent firing
- sympathetic stimulation to cause increase TPR
- coronary vasodilation (by what mechanism?)

Why is there a vasodilators vs vasoconstrictive action?

Thanks a lot in advance.

 

[Pinkleton]

I'm confused. I thought that hypoxia resulted in systemic vasodilation and pulmonary vasoconstriction. But you are saying that it causes systemic vasoconstriction?

As far as coronary vasodilation is concerned, I think that is determined by local metabolites like CO2 which have a vasodilatory effect in most tissues. But why would low O2 (i.e. in anemia) result in elevated metabolites is what I'm now wondering...?

 

[Sir Gillies]

Thanks for your reply. That's why I posted this issue, because I came across it on a physiology website (which I don't have link unfortunately) and wrote it down.

I agree that hypoxia induces pulmonary vasoconstriction and that coronary circulation autoregulation is mainly mediated by local metabolites. But I wanted to check with someone smarter than me what exactly happens in the systemic circulation (vasodilation or constriction?) in case of hypoxia/hypercapnia.

I hope someone can help.

 

[Pinkleton]

After thinking about it some, here's my best guess at what's happening.

With tissue HYPOXIA such as in exercising cardiac and skeletal muscles, local metabolic control (the most important control for these tissues) dominates over all other effects and you have vasodilation. Here, you don't have hypoxemia so you PO2 is normal. Since the total cross sectional area of these tissues is so large, you will have a drop in TPR

With HYPOXEMIA where your PO2 drops, you have the situation that you described. You will have increased TPR and BP in most tissues. The organs that escape this effect using autoregulation would be the brain, heart, and kidneys; blood flow must always remain constant in these tissues. So in effect, you are shunting blood from less important areas to critical areas because you have no oxygen to waste

This would make sense because the chemoreceptors are located in the carotid and aortic bodies, making them sensitive to hypoxemia, not hypoxia. Whereas local effects are regulated by tissues themselves, making them sensitive to hypoxia and not hypoxemia

 

[Zedor]

Am I correct in saying that BP is mainly controlled by baroreceptors. But chemoreceptors also may play role and if not influenced by respiratory modulation, then hypoxia (or hypercapnia/acidosis) causes:
- Decrease firing of peripheral chemoreceptors
- decrease afferent firing
- sympathetic stimulation to cause increase TPR
- coronary vasodilation (by what mechanism?)

Why is there a vasodilators vs vasoconstrictive action?

Thanks a lot in advance.

I'm not sure, but I believe that chemoreceptors are usually a last ditch effort when you are in hemorrhagic shock (in regards to cardiovascular control). The baroreceptors are usually sufficient until MAP falls sufficiently low that (60 mmHg?). As such, the heart's activity increases in an attempt to maintain MAP, and the increased work of the heart is what drives coronary vasodilation. I'm not sure if that's right, but that makes sense in my head.

 

[Pinkleton]

Bump. Anyone mind clearing this up? I feel like I've forgotten everything from our cardio block 😕

 

[SpecterGT260]

Am I correct in saying that BP is mainly controlled by baroreceptors. But chemoreceptors also may play role and if not influenced by respiratory modulation, then hypoxia (or hypercapnia/acidosis) causes:
- Decrease firing of peripheral chemoreceptors
- decrease afferent firing
- sympathetic stimulation to cause increase TPR
- coronary vasodilation (by what mechanism?)

Why is there a vasodilators vs vasoconstrictive action?

Thanks a lot in advance.

So quick changes in BP are mostly regulated by baroreceptors (carotids respond on a continuum and can increase or decrease BP by affecting both para and sympathetic output via CN IX, although its sympathetic impact is probably mediated through parasymp loops. the Aorta only responds to spikes and can lower BP by affecting parasympathetic tone through CN X).

You are right in saying that sympathetic tone impacts TPVR. Baroreceptors will impact this (I believe) as will adrenal secretions and... other things. There is also local vascular control via NO and metabolite balances, but these do not really impact arterial BP.

Chemoreceptors have much more to do with your pH and acid-base balance than they do your BP. There are downstream effects of aberrant chemo function that can mess with BP in a secondary manner. Catecholamine release is a big one, although I am not sure what the exact mechanism is. May be triggered by the brain chemo-sensing areas or it may be something to do with the physiology of symp neurons as ion imbalances can mess with this. The chemoreceptors in the carotids and aorta have more to do with breathing regulation than they do TPVR. That said, IIRC there is another reflex loop that increases HR with increased RR and that would increase BP. Both the baroreceptors and chemo receptors send afferents to the NTS in the brain stem, but they hit different areas and have different outputs. The Nucleus Ambiguous outputs to both lungs and the CV system. According to my notes direct stimulation of 1 type of receptor will have a predominant effect of only the primary type (chemo = resp, baro = TPVR, CO) but its the brainstem, which is a giant tangled ball of mess and nonsense, so I don't have down if 2* effects are reflex mediated or directly mediated by the receptor.

Coronary circulation is entirely controlled locally. Metabolites are given off by heart muscle which triggers coronary vasculature to dilate. It is probably important to also note here that the heart always fully depletes its blood supply so the pH shift within the muscle won't help with oxygenation. Anything it will do here is to dilate vessels. I presume this is why "coronary steal syndrome" is a problem here where you don't hear about it as often in other areas of the body. While other vessels have sympathetic input mediating their tone, the coronary arteries only care about what they see within them and don't care at all about the segment of vessel 1/2 inch behind, in front of, or beside them.

Let me know if I have anything backwards or said anything goofy. But I think this should be accurate.