Acetylcholine and heartrate

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HereWeGo21

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So I got a Kaplan question saying that Ach administration INCREASES heart rate?

I now get the mechanism they're going for. Ach --> peripheral vasodilation --> reflex tachycardia.

But...like...what about the M2 muscarinic receptor on the heart?? Wouldn't Ach directly cause bradycardia by acting on that receptor? Like, I'm having a hard time imagining that the reflex would win out over the direct stimulation. Can anyone speak to this? In general, is there a good system for determining whether reflex or direct effect wins? Thanks

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Vessels rule , heart follows..

Edit: just think of the little Gi receptor having to fight the whole orchestrated sympathetic response , not much of a chance to win..
 
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So I got a Kaplan question saying that Ach administration INCREASES heart rate?

I now get the mechanism they're going for. Ach --> peripheral vasodilation --> reflex tachycardia.

But...like...what about the M2 muscarinic receptor on the heart?? Wouldn't Ach directly cause bradycardia by acting on that receptor? Like, I'm having a hard time imagining that the reflex would win out over the direct stimulation. Can anyone speak to this? In general, is there a good system for determining whether reflex or direct effect wins? Thanks
Wait, what huh?? Acetylcholine would not have effects on the vasculature. What receptors were you considering? There are no cholinergic nerves in the vasculature... (unless we're talking about erectile tissue)

Acetylcholine would have action at the Sympathetic ganglion where preganglionic sympathetic nerves release ACh to activate Nicotinic cholinergic receptors in their effector organ (adrenal medulla) to cause the release of epinephrine into the blood (hormone). The epinephrine would activate the heart through Beta-1 adrenergic receptors to increase heart rate, and also stimulate the vasculature through mostly Alpha-1 (vasoconstriction) and the airways to dilate through Beta-2 in the bronchial smooth muscle.
 
There are M3 Gq GPCreceptors in vasculature that are NOT innervated and coupled to eNOs --> direct stimulation by Injcted ACh --> vasodilation . They probably have no physiologic role , but Kaplan fancies them
 
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