Chronic effects of ACTH and cortisol excess on arterial pressure in normotensive and hypertensive dogs.
- 1 September 1982
- journal article
- research article
- Published by Wolters Kluwer Health in Hypertension
- Vol. 4 (5) , 652-661
- https://doi.org/10.1161/01.hyp.4.5.652
Abstract
The chronic effects of ACTH and cortisol on mean arterial pressure (MAP) and related variables were studied in normotensive dogs and, subsequently, in the same dogs after they were made hypertensive by chronic infusion of angiotensin II (AII). MAP was recorded continuously, 24 h/day, and Na intake was 71 meq/day. In both normotensive and hypertensive dogs, 8-10 days of ACTH infusions caused natriuresis, kaliuresis, diuresis, hypernatremia and hypokalemia; additionally, plasma renin activity (PRA) was suppressed to undetectable levels. During ACTH infusion, there was a sustained 12-fold increase in plasma cortisol concentration, but only a transient elevation in plasma aldosterone concentration; this steroidogenic response occurred even in dogs with AII hypertension where plasma AII concentration was maintained at elevated levels by infusion. In normotensive dogs, increases in MAP were not consistently observed during ACTH infusion, whereas, in dogs with AII hypertension, ACTH invariably exacerbated the hypertension .**GRAPHIC**. = +16 mm Hg). Cortisol infusion, like ACTH infusion, caused a 12-fold increase in plasma cortisol concentration, and negative Na and water balance; however, cortisol did not produce kaliuresis, hypokalemia, suppression of PRA or hypertension. Cortisol induced chronic hypotension .**GRAPHIC**. = -7 mm Hg) when infused in normotensive dogs, and in dogs with AII hypertension, there were no detectable changes in MAP during cortisol treatment. The changes in plasma cortisol concentration and PRA that accompany ACTH infusion do not mediate, but seem actually to oppose, the hypertensive effects of ACTH. When ACTH was infused in hypertensive dogs with fixed plasma levels of AII, the hypertensive effect of ACTH were manifested. Failure of chronic ACTH administration to maintain an elevated secretion rate of aldosterone cannot be attributed to suppression of PRA. [The involvement of ACTH and adrenocortical hormones in the hypertension found in Cushing''s syndrome is discussed.].This publication has 38 references indexed in Scilit:
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