molec bio/physio question

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HiddenTruth

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I am trying to put this together, but wanted to hear your guys' thoughts.

So, M3 activation (e.g pilocarpine mediated vasodilation of vasc sm mm) and H1 mediated vasodilation are via NO synthesis (Increased cGMP-->dephosp of myosin light chain-->prevent actin-myosin interaction). But, then both of these receptors also mediate increase in intracellular Ca++ via IP3, etc, which theoretically should result in contraction, no? I'm apparently not putting this together somehow, or maybe it's not meant to be put together like this. 😕

Also, I don't quite understand how B2 mediated relaxation of vasc sm mm via increase in camp works? It says M2 activ--> decrs cAMP, which opens K+ channels and leads to hyperpol (so this is referring to phase 3 of the AP in SA/AV nodes)? Somehow when i think of "relax" or "slowing" (like parasymp actions), i clump them together, but clearly in this example, one is increasing camp, and the other is decreasing camp.

It seems as if there is inconsistency between the responses produced by different receptors and their molecular pathways. Sorry, I think the way I have written this may be confusing, but if someone can help me straighten these pathways out, I'd appreciate it. Thanks.
 
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