Sodium-sensitive hypertension. Implications of pathogenesis for therapy |
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Authors: | N K Hollenberg G H Williams |
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Affiliation: | Department of Medicine, Harvard Medical School, Boston, MA. |
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Abstract: | Fifty to sixty percent of clinical hypertension is sensitive to sodium (Na) intake: known causes, primary aldosteronism, bilateral renal artery stenosis, mild azotemia, acromegaly, and low-renin hypertension account for only a fraction. We have identified a group of normal-renin hypertensives characterized by inability to modulate normally their renal vascular and adrenal responsiveness to angiotensin II. These patients handle shifts in Na intake abnormally, show more positive balance on a high-salt diet, and raise their blood pressure when shifted to a high-salt diet. Renal blood flow does not shift with Na intake, but does respond strikingly to converting enzyme inhibition, which also corrects altered renal and adrenal responsiveness, ability to handle a sodium load, and hypertension. These patients have a striking family history of hypertension; 50% of the offspring of hypertensives show similar features, including a renal vasodilator response to converting enzyme inhibitors or calcium channel blocking agents. Accumulating evidence suggests that the abnormality is inherited and may be the most common form of hypertension. |
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