why stimulate Gq receptors with AT-II?

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AndreyE

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We know that AT-II type 1 receptors are Gq-coupled. Which causes vasoconstriction.
Now tell me why in the world we want to stimulate these receptors in hypertension and CHF?
There is something important wiki-pedia hides. I guess it's about tissue distribution?
 
Now tell me why in the world we want to stimulate these receptors in hypertension and CHF?

We don't want to stimulate receptors in patients with htn or chf, which is why we either block the synthesis of AT with ACE-I, or we block their action with ARB in patients who can't tolerate ACE-I.

If you are asking why the body itself may release more angiotensin in the setting of chf, that's because the effective arterial blood volume is reduced due to a reduction in cardiac output, which stimulates the kidneys to release renin ->>> increased angiotensin production.
 
Thanx a lot, apperantly I've been thinking about Formula-1 too much and my mind numerously skipped "antagonists" when I had been reading about AT-II receptors type 1 in wikipedia....

Now it's very much clear.... so if I have elderly patient in acute heart failure I believe ACE inhib intravenously\sublingv is obligatory? I guess if I don't want to provoke a heart attack in any dehydrated patient I could possibly go with ACE too?
 
Now it's very much clear.... so if I have elderly patient in acute heart failure I believe ACE inhib intravenously\sublingv is obligatory? I guess if I don't want to provoke a heart attack in any dehydrated patient I could possibly go with ACE too?

No prob. But, no, you would not use an ACEI for acute heart failure, as it is not a strong diuretic. For decompensated HF you would use IV lasix, morphine, and nitrate, plus oxygen, and position them sitting up. For longer term advanced hf you would use iv vasodilators and an inotrope such as dobutamine etc. This is beyond what you need to know for step one though - just know the RAS system, AT effects on the kidney in particular, and vasculature in general (including bradykinin interaction), g coupling, methods of synthesis, and drugs that affect it. That's all. 😉

I actually don't know why I'm in the step 1 forum...clicked on the wrong bookmark and didn't realize until I'd already replied. 😛
 
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