Nitric Oxide in Hypertension - How to Heal ?

 Abstract

 Evidence suggests that NO plays a major role in regulating blood pressure and that impaired NO bioactivity is an important component of hypertension. Mice with disruption of the gene for endothelial NO synthase have elevated blood pressure levels compared with control animals, suggesting a genetic component to the link between impaired NO bioactivity and hypertension. 



Hypertension is a major risk factor for cardiovascular disease, and reduction of elevated blood pressure significantly reduces the risk of cardiovascular events. Endothelial dysfunction, which is characterized by impairment of nitric oxide (NO) bioavailability, is an important risk factor for both hypertension and cardiovascular disease and may represent a major link between the conditions.


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Hypertension - Clinical Studies

 Impaired NO bioactivity is also implicated in arterial stiffness, a major mechanism of systolic hypertension. Clarification of the mechanisms of impaired NO bioactivity in hypertension could have important implications for the treatment of hypertension.

Clinical studies have shown that patients with hypertension have a blunted arterial vasodilatory response to infusion of endothelium-dependent vasodilators and that inhibition of NO raises blood pressure.


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Experimental data in humans are limited. While most data are consistent with the results obtained in animal models, others have found no evidence for a role of NO in the regulation of sympathetic outflow. In one study, the BP increase observed with NO inhibition via l-NMMA infusion in healthy human subjects was accompanied by significant decreases in heart rate and MSNA, which were similar to the effects of infusion of phenylephrine (anNO-independent vasoconstrictor), suggesting no apparent effect of NO on central sympathetic outflow. 96 Another study found that while l-NMMA infusion raised BP in 8 healthy subjects, the exercise-induced increase in MSNA during head-up tilt was similar with and without l-NMMA infusion. 97 In contrast, a study in 15 healthy male volunteers found that infusion of l-NMMA at rest increased BP significantly but had no effect on MSNA, while phenylephrine infusion resulted in a similar BP increase; a 50% decrease in MSNA was also documented, probably evoked by the baroreflex response to increased BP. Hence, NO blockade appeared to counteract this sympathetic response (Figure 5) .98 


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When sodium nitroprusside was coinfused with l-NMMA, the increase in BP was abolished, but MSNA increased significantly. These findings suggest that inhibition of NO had sympathoexcitatory effects that were masked by the inhibitory response of the baroreflexes, providing the first indication that NO regulates central SNS outflow in humans and that neuronal NO as well as endothelial NO mediate vasomotor tone.


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