Journal
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION
Volume 11, Issue 2, Pages 197-200Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00041552-200203000-00011
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- NHLBI NIH HHS [HL-55006] Funding Source: Medline
- NIDDK NIH HHS [DK-15843, DK-52617] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P50HL055006] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK015843, P50DK052617] Funding Source: NIH RePORTER
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Long-term control of arterial pressure has been attributed to the kidney by virtue of its ability to couple the regulation of blood volume to the maintenance of sodium and water balance by the mechanisms of pressure natriuresis and diuresis. In the presence of a defect in renal excretory function, hypertension arises as the consequence of the need for an increase in arterial pressure to offset the abnormal pressure natriuresis and diuresis mechanisms, and to maintain sodium and water balance. There is growing evidence that an important cause of the defect in renal excretory function in hypertension is an increase in renal sympathetic nerve activity (RSNA). First, increased RSNA is found in animal models of hypertension and hypertensive humans. Second, renal denervation prevents or alleviates hypertension in virtually all animal models of hypertension. Finally, increased RSNA results in reduced renal excretory function by virtue of effects on the renal vasculature, the tubules, and the juxtaglomerular granular cells. The increase in RSNA is of central nervous system origin, with one of the stimuli being the action of angiotensin II, probably of central origin. By acting on brain stem nuclei that are important in the control of peripheral sympathetic vasomotor tone (e.g. rostral ventrolateral medulla), angiotensin II increases the basal level of RSNA and impairs its arterial baroreflex regulation. Therefore, the renal sympathetic nerves may serve as the link between central sympathetic nervous system regulatory sites and the kidney in contributing to the renal excretory defect in the development of hypertension. Curr Opin Nephrol Hypertens 11:197-200. (C) 2002 Lippincott Williams Wilkins.
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