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Reinforces established NO mechanisms in hypertension; leaves open targeted therapies pending prospective clinical validation.
Although hypertension has been studied extensively for decades, its etiology remains an enigma. An increase in systemic intravascular pressure or systemic hypertension can result from changes in two basic hemodynamic parameters: (1) a decrease in intravascular size as occurs during vasoconstriction, or (2) an increase in intravascular volume. The latter may occur as a result of either increased salt and water retention or cardiac output. Nitric oxide (NO·) has emerged as a critically important agent in the regulation of vascular tone, renal fluid and volume regulation, and cardiac function. Consequently, an alteration in NO· action on vessel tone, volume regulation, or heart function can lead to hypertension (Fig. 1).
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Rudd et al. (2000) studied this question.
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