Clinical and Experimental Hypertension Part A Theory and Practice · 1982 · 28 citations · 19 references
MedicineEndocrinologyObstetricsHormone BiochemistryReproductive EndocrinologySteroid BiochemistryAdrenal DisordersAdrenal HormonesHypertensive DisordersPregnancyPregnancy EndocrinologyPregnancy-induced HypertensionAldosterone BiosynthesisAldosterone MetabolismAldosterone PhysiologyAldosterone ReceptorsAldosterone RegulationPlasma Renin ActivityPregnancy-induced Hypertension PhysiologyPrimary Aldosteronism Localization
Serial measurements of plasma renin activity, plasma progesterone and urinary aldosterone were made before, during and after pregnancy in a patient from whom an A-P-A was later removed with cure of hypertension and hypokalemia. Despite 16-fold increases in urinary aldosterone during pregnancy, plasma renin activity levels became unsuppressed, and hypertension and hypokalemia were reversed. Increases in plasma progesterone or other steroids, competitively inhibiting the effects of aldosterone on its receptor, may explain remission of A-P-A and reversal of renin suppression during pregnancy. In a second patient, the features of primary aldosteronism appeared immediately after a pregnancy, and removal of an A-P-A cured hypertension and hypokalemia. A-P-A is more common in females and may appear following pregnancy. Urinary aldosterone was 6-fold higher after pregnancy than before. Thus, sex steroids may not only protect from hyperaldosteronism but may also stimulate growth of A-P-A's.
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Edgar Haber, THERESA KOERNER, Lot B. Page et al. · The Journal of Clinical Endocrinology & Metabolism · 1969 · 2.2K citations · Full text
Craig A. Winkel, Leon Milewich, C. Richard Parker et al. · Journal of Clinical Investigation · 1980 · 107 citations · Full text