bayraktutan u, yang z-k, shah am (1998) selective dysregulation of nitric oxide synthase type 3 in cardiac myocytes but not coronary microvascular endothelial cells of spontaneously hypertensive rats. cardiovasc res 38:719–726

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Nitric oxide produced inside the heart through nitric oxide synthase is a fairly reactive signaling molecule and a crucial modulator of the myocardial features.

NOS catalyzes the conversion of L-arginine to L-citrulline and NO however under particular circumstances reactive oxygen species can be shaped as opposed to NO uncoupling. in the heart, three isoforms are a gift  neuronal and endothelial  are constitutively present enzymes in distinct subcellular places within cardiomyocytes, while inducible  is absent in the wholesome coronary heart

Its expression is brought about by means of seasoned-inflammatory mediators. inside the tissue, NO has two predominant consequences first NO stimulates the pastime of guanylate cyclase, main to cGMP era and activation of protein kinase G, and 2nd NO nitrosylates tyrosine and thiol-groups of cysteine in proteins. Upon nitrosylation, proteins may additionally trade their homes. changes in first NOS expression and interest 2nd subcellular compartmentation of NOS pastime, and third the prevalence of uncoupling can also cause a couple of NO-triggered results.

Some of these are particularly obvious at some point of myocardial overload as take place at some point of aortic constriction and myocardial infarction. a lot of those NO-brought-on consequences are considered to be cardioprotective but especially if NOS will become uncoupled, the formation of ROS in combination with a low NO bioavailability predisposes for cardiac damage.

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