Cardiovascular system endothelium

Fedisdi M (1991) Ihe action and metabolism of organic nitrates and their similarity with endothelium-derived rdaxing fa (EDRF). hi Moncada S, Higgs EA, Berrazueta IR eds. Clinical rdevance of nitric oxide in the cardiovascular system, Edioomplet Madrid, pp. 29-43... 

Vasopressin also is a potent vasopressor whose name was chosen in recognition of its vasoconstrictor action. Vasopressin is a neurotransmitter among its actions in the CNS are apparent roles in the secretion of ACTH and in the regulation of the cardiovascular system, temperature, and other visceral functions. Vasopressin also may play a role in hemostasis by promoting the release of coagulation factors by the vascular endothelium and increasing platelet aggregation. 

NO synthesized by eNOS cells, diffuses out in all directions. About 80 to 90% of NO released by the endothelium in the cardiovascular system is washed away by the blood, where it is used to prevent platelet aggregation and the subsequent formation of blood clots. The remaining amount of NO diffuses to the wall (smooth muscle) of arteries and veins and triggers a cascade of events leading to the production of cyclic GMP and smooth muscle relaxation. Relaxation of the smooth muscle allows the blood vessel to dilate (increase of vessel diameter), resulting in lowered blood pressure. The cardiovascular system maintains a constant level of NO at a given blood flow [27]. When blood flow increases, the endothelium releases more NO to maintain its constant concentration in the blood stream. When this normal level is not produced, either because production is blocked by administration of eNOS inhibitors or by pathological states such as deposition of cholesterol on the wall of the arteries (atherosclerosis), the vascular muscles do not relax to the... 

Numerous studies indicate that regular intake of polyphenol-rich food and beverages such as red wine is associated with a protective effect on the cardiovascular system. In addition to the antioxidant property, polyphenols may also induce a beneficial effect on the cardiovascular system by several other mechanisms including the improvement of the vascular function. Indeed, experimental and chnical studies indicate that polyphenols are potent inducers of two major endothelial vasoprotective mechanisms, the formation of nitric oxide (NO) and the induction of endothelium-derived hyperpolarization (EDH). 

AVP is synthesized in the fetal hypothalamus. In addition to its role in altering gene expression (e.g., POMC), plasma AVP levels also increase in response to fetal hypoxia-ischemia (30,70,71). The release of AVP is not mediated by peripheral chemoreceptor mechanisms and therefore is unlikely to contribute to the rapid cardiovascular changes at the onset of hypoxia (see above) (30). Exogenously administered AVP produces hypertension, peripheral vasoconstriction, and bradycardia (71-73), although the contribution of hypoxia-stimulated increases in AVP to the redistribution of fetal CVO is uncertain (74,75). Endothehal VI receptors mediate an AVP vasodUatory effect, which means that the net effect of AVP on the cardiovascular system is likely to reflect an integrated picture of vasoconstriction from a number of vascular beds, modulated by endothelium-dependent vasodUatory mechanisms (76). 

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