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Cyclic guanosine monophosphate (cGMP) is a cyclic nucleotide derived from guanosine triphosphate (GTP). cGMP acts as a second messenger much like cyclic AMP.Its most likely mechanism of action is activation of intracellular protein kinases in response to the binding of membrane-impermeable peptide hormones to the external cell surface. [1]
The elevation of intracellular cGMP results in relaxation by the activation of cGMP-dependent protein kinase, which phosphorylates target proteins such as the myosin phosphatase-targeting subunit (MYPT) and the IP3 receptor-associated cGMP kinase substrate (IRAG). In addition, cGMP has been proposed to also cause smooth muscle relaxation ...
Endogenous substances and drugs that cause vasodilation are termed vasodilators. Many of these substances are neurotransmitters released by perivascular nerves of the autonomic nervous system [ 6 ] Baroreceptors sense blood pressure and allow adaptation via the mechanisms of vasoconstriction or vasodilation to maintain homeostasis .
The nitric oxide will then diffuse into the vascular smooth muscle and will activate the soluble guanylyl cyclase. The subsequent increase in cGMP will cause vasodilation with the same effects as described above. This is why nitroglycerine is given to a person having a heart attack. The nitroglycerine will be metabolized to nitric oxide, which ...
In smooth muscle, cGMP is the signal for relaxation, and is coupled to many homeostatic mechanisms including regulation of vasodilation, vocal tone, insulin secretion, and peristalsis. Once formed, cGMP can be degraded by phosphodiesterases , which themselves are under different forms of regulation, depending on the tissue.
cGMP-dependent protein kinase or protein kinase G (PKG) is a serine/threonine-specific protein kinase that is activated by cGMP. It phosphorylates a number of biologically important targets and is implicated in the regulation of smooth muscle relaxation, platelet function, sperm metabolism, cell division , and nucleic acid synthesis.
However, with respect to vasculature, activation of M 3 on vascular endothelial cells causes increased synthesis of nitric oxide, which diffuses to adjacent vascular smooth muscle cells and causes their relaxation and vasodilation, thereby explaining the paradoxical effect of parasympathomimetics on vascular tone and bronchiolar tone.
Cilostazol is approved for treatment of intermittent claudication and is thought to involve inhibition of platelet aggregation and also inhibition of smooth muscle proliferation and vasodilation. The most studied roles of PDE3B have been in the areas of insulin , IGF1 , and leptin signaling. [ 1 ]