The Response of Metabolic Alkalosis in Severe Hypertension to Antihypertensive Drugs

Publisher Website
Google Scholar
Abstract
Severe hypertension was discovered in a 34-year-old white man known to have been normotensive 1 year before study. Headache, moderate polyuria and early fatigue were present for 10 weeks. Grade IV hypertensive retinopathy and 2+ proteinuria were found on admission. During a 14-day pretreatment period of evaluation the average diastolic pressure exceeded 140 mm Hg, serum Kaveraged 3.2 mEq/liter and serum CO, content averaged 32.3 mM/liter. Serum Na and urea N were normal. The persistent metabolic alkalosis was not associated with pre-hospitalization drug therapy, dietary aberration, gastro-intestinal disorder, or overt endocrine disease. Urinary aldosterone excretion was in the mid-normal range. Treatment with guanethidine and hydralazine promptly reduced his blood pressure, and there was simultaneous improvement in the alkalosis. Serum electrolytes returned to normal within 7 days, and polyuria decreased after 3 weeks. Alkalosis did not reappear after subsequent addition of chlorothiazide, 1 g daily to the drug regimen. Other data support the view that significant metabolic alkalosis occurs infrequently as a concomitant of severe hypertension. The alkalosis is probably induced by a renal mechanism. Activation of renin-angiotensin-aldosterone pathway is a plausible explanation, but the pathophysiologic background of this clinical category of metabolic alkalosis is still uncertain.