Sodium-sensitive hypertension. Implications of pathogenesis for therapy.
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.
Hollenberg
N K
NK
Department of Medicine, Harvard Medical School, Boston, MA.
Williams
G H
GH
D000311:Adrenal Glands / Q000378:metabolism; D000450:Aldosterone / Q000378:metabolism; D000804:Angiotensin II / Q000502:physiology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D004039:Diet, Sodium-Restricted; D004198:Disease Susceptibility; D006801:Humans; D006973:Hypertension / Q000139:chemically induced* / Q000188:drug therapy / Q000235:genetics; D007668:Kidney / Q000502:physiology; D012079:Renal Circulation; D012965:Sodium Chloride
D000806:Angiotensin-Converting Enzyme Inhibitors; D000804:Angiotensin II; D012965:Sodium Chloride; D000450:Aldosterone