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 . 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).
Was this article helpful?
The term vaginitis is one that is applied to any inflammation or infection of the vagina, and there are many different conditions that are categorized together under this ‘broad’ heading, including bacterial vaginosis, trichomoniasis and non-infectious vaginitis.