Endothelial Function in Hypertension: Role of Nitric Oxide

Nitric oxide (NO) is the endogenous vasodilator produced by the endothelium. Although NO release seems to be influenced by changes in blood pressure, whether its production is or not affected in hypertension has been very controversial. Recent research work is showing the existence of profound differences in the role of NO in hypertension. This role seems to vary depending on the class of hypertension. In spontaneous and renovascular hypertension, the production of NO is increased probably as a compensatory mechanism. However, in genetic hypertension NO is inefficacious, presumably because of increased inactivation by oxidative radicals. In this form of hypertension an increased production of contractile factors or a decreased release of hyperpolarizing factors seems to be involved. In salt-dependent hypertension, NO production is impaired probably due to a deficiency of the substrate for NO synthase. In human hypertension, pharmacological experiments reveal an impaired NO dilator mechanism. In pulmonary hypertension, the use of NO gas inhalation has been proposed as a future therapy for this condition. This chapter reviews the evidence, concentrating on the evidence from animal models.