Nitric Oxide

Vascular nitric oxide (NO) plays a key role in the regulation of blood pressure and tissue perfusion. There is considerable evidence supporting the presence of NO-mediated signaling in cerebral arteries, where it contributes particularly to the maintenance of basal CBF. Although a wide variety of modulators of cerebral vasomotor function exist in addition to NO (e.g. endogenous peptides such as bradykinin and endothelins; and molecules related to the enzymatic activity of cyclooxygenase, heme-oxygenase, and superoxide dismutase), the actions of most of these are linked in one way or another to NO itself [1]. Therefore, an understanding of NO-mediated signalling is essential to the study of cerebrovascular physiology and pathophysiology.

Vascular NO signal transduction involves the following: (1) a principal mediator, i.e. molecular NO; (2) a well defined biosynthetic apparatus for NO, i.e. the enzyme nitric oxide synthase (NOS); (3) and an effector pathway and cellular target, namely the NO-activated enzyme guany-late cyclase and the second messenger molecule cyclic 3'5'-guanosine monophosphate (cGMP), located within vascular smooth muscle cells (Figs 17.1 and 17.2).

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Cure Your Yeast Infection For Good

Cure Your Yeast Infection For Good

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