Figure 1417

Major organ, A, and cellular, B, targets of nitric oxide (NO). A, Synthesis and function of NO. B, Intracellular targets for NO and pathophysiological consequences of its action. C, Endothelium-dependent vasodilators, such as acetylcholine and the calcium ionophore A23187, act by stimulating eNOS activity thereby increasing endothelium-derived nitric oxide (EDNO) production. In contrast, other vasodilators act independently of the endotheli-um. Some endothelium-independent vasodilators such as nitroprus-side and nitroglycerin induce vasodilation by directly releasing nitric oxide in vascular smooth muscle cells. NO released by these agents, like EDNO, induces vasodilation by stimulating the production of cyclic guanosine monophosphate (cGMP) in vascular smooth muscle (VSM) cells. Atrial natriuretic peptide (ANP) is also an endothe-lium-independent vasodilator but acts differently from NO. ANP directly stimulates an isoform of guanylyl cyclase (GC) distinct from soluble GC (called particulate GC) in VSM. CNS—central nervous system; GTP—guanosine triphosphate; NOS—nitric oxide synthase; PGC—particulate guanylyl cyclase; PNS—peripheral nervous system; ROI—reduced oxygen intermediates; SGC—soluble guanylyl cyclase. (A, From Reyes et al. [9], with permission; B, from Kim et al. [10], with permission.)

0 0

Post a comment