Recurrence of hypertension in primary aldosteronism after discontinuation of spironolactone. Time course of changes in cardiac output and body fluid volumes.
Hemodynamic mechanisms underlying the hypertensive action of long-standing sodium overload were studied in ten subjects with aldosterone-producing adenoma. Arterial pressure was 129+/-4/91+/-4 mm Hg (mean+/-SEM) during spironolactone treatment, 177+/-5/114+/-3 mm Hg six weeks after the drug had been stopped, and 136+/-4/94+/-3 mm Hg two months after operation. In the six weeks following cessation of spironolactone, cardiac output, stroke volume, blood volume and sodium space were determined at weekly intervals. In each subject the biochemical syndrome of aldosterone-excess had been fully developed in two weeks. The hemodynamic changes in that period were also uniform. Mean arterial pressure in week 2 was increased by 20+/-3% with parallel increments of cardiac output and stroke volume of 22+/-5 and 30+/-6%. Blood volume and sodium space were increased by 11+/-2 and 29+/-4%. The patterns in weeks 2-6 were not uniform. In five subjects (age 33-49 yr) the hypertension was maintained through increased cardiac output; in week 6 it was 34+/-7% above its initial value, and stroke volume and blood volume were 37+/-4 and 16+/-4% above control. In the remaining five subjects (age 50-60 yr) cardiac output, stroke volume and blood volume returned to their initial values, and total peripheral resistance in week 6 was 36+/-13% above control. Sodium space remained expanded in both groups. The measurements after surgery confirmed the existence of the high-flow and high-resistance patterns; there was a decrease in cardiac output in the former group of subjects and a decrease in resistance in the latter. Apparently, increased resistance is not a direct consequence of increased flow. The observed age-related differences in hemodynamic patterns of sodium overload bear some resemblance to essential hypertension where a high-flow state of long duration may precede the ultimate phase of low vascular capacitance and high resistance.
D000450:Aldosterone / Q000097:blood*; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D006801:Humans; D006929:Hyperaldosteronism / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D011188:Potassium / Q000097:blood; D012083:Renin / Q000097:blood; D012964:Sodium / Q000097:blood; D013148:Spironolactone / Q000627:therapeutic use*; D014882:Water-Electrolyte Balance / Q000187:drug effects
D013148:Spironolactone; D000450:Aldosterone; D012964:Sodium; D012083:Renin; D011188:Potassium