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Old 12-27-2012
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Kaplan Medical error in kaplan pharmac lecture notes anti anginal drugs

I just noticed this blatant error in Kaplan lecture notes in the anti anginal drugs chapter.

If you take figure III-5-2 (Mechanisms of smooth muscle contraction and relaxation and drugs affecting them) (2010 version of notes)

In bottom left corner of the figure, they have shown that bradykinin, H1, M3 act via Gq coupled receptors, which then increase NO leading to activation of guanyl cyclase.

But doesnt Gq receptors act via PIP2 system (IP3, DAG).

So isnt this wrong? Or am i wrong?

Then by what molecular mechanism does m3,h1 and bradykinin cause relaxation of smooth muscle?
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Old 01-12-2013
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That's only part of the answer. When Calcium is released via the PIP2 DAG pathway, it in turn binds to Calmodulin. This activates eNOS (endothelial Nitric Oxide synthase) which then proceeds to bind activate Guanyl cyclase and increase cGMP, causing relaxation.
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Old 12-04-2013
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hey, it`s been long time since you discussed this but i didn`t quite understand ashratnam reply
"When Calcium is released via the PIP2 DAG pathway, it in turn binds to Calmodulin. This activates eNOS (endothelial Nitric Oxide synthase) which then proceeds to bind activate Guanyl cyclase and increase cGMP, causing relaxation."

but in the same time Gq ->phospholipase C -> DAG,PIP2,Ca2+ ->protein kinase C ->vasoconstriction

so what does Gq do constrict or relax?
(it suppose to contstrict, doesn`t it?)
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Old 12-04-2013
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Quote:
Originally Posted by jeniaz View Post
hey, it`s been long time since you discussed this but i didn`t quite understand ashratnam reply
"When Calcium is released via the PIP2 DAG pathway, it in turn binds to Calmodulin. This activates eNOS (endothelial Nitric Oxide synthase) which then proceeds to bind activate Guanyl cyclase and increase cGMP, causing relaxation."

but in the same time Gq ->phospholipase C -> DAG,PIP2,Ca2+ ->protein kinase C ->vasoconstriction

so what does Gq do constrict or relax?
(it suppose to contstrict, doesn`t it?)

Protein kinase c phosphorylase a set of tissue- specific substrate enzymes. So depending on the enzyme in consideration we have the effect. So in this case endothelial derived nitric oxide synthase eNOs. when its phosporylated becomes active working through the NO pathway increasing cGMP leading to dephosphorylation of myosin light chain kinase so that it cannot bind actin and so causing relaxation. so the H1 and M1 receptors working through Gp pathway would lead to vasodilation. So Gp pathway does not always vasoconstrictor. If it works through alpha 1 and angiotensin 2 as we all know then it would vasoconstrictor.
Hope it helps.
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