Endocrinology, Vol 137, 4773-4778, Copyright © 1996 by Endocrine Society

ARTICLES

Effect of progesterone on aldosterone secretion in rats

LM Braley, AI Menachery, T Yao, RM Mortensen and GH Williams
Endocrine-Hypertension Division, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

In both human and animal studies high progesterone states are associated with elevated aldosterone production but variable changes in PRA. These experiments were designed to test the hypothesis that progesterone has an effect similar to a low sodium diet on the glomerulosa cell: increasing aldosterone synthase messenger RNA activity and aldosterone production. Ovariectomized (OVX) rats were injected with progesterone (1 mg/100 g) or vehicle (SHAM) for 5 days. In a separate study, intact rats were placed on a low (0.02%) or high (1.6%) sodium diet for 5 days. On the day of death, rats were decapitated and blood collected for serum hormone determinations. Isolated adrenal glomerulosa cells were incubated +/- 10 nM angiotensin II (A II), after which aldosterone and corticosterone were measured. Early (conversion of cholesterol to pregnenolone) and late (conversion of corticosterone to aldosterone) aldosterone pathway activity was assessed in parallel incubates by adding cyanoketone and excess corticosterone with subsequent measurement of pregnenolone and aldosterone. In vivo, progesterone administration, like dietary sodium restriction, caused a significant increase in PRA (p < or = 0.043) and plasma aldosterone (p < or = 0.009), with no change in plasma corticosterone. Additionally, both treatments caused a significant increase in baseline (P < or = 0.01) and A II-stimulated (p < or = 0.027) aldosterone secretion in vitro. This increased responsiveness was secondary to activation of late pathway activity (p < or = 0.022) as determined by both an increased conversion of corticosterone to aldosterone and by an increase in messenger RNA levels of the late pathway enzyme aldosterone synthase. Thus, chronic progesterone administration apparently does not directly influence aldosterone secretion, but rather acts indirectly to increase aldosterone by mechanisms similar to sodium restriction.

This article has been cited by other articles:

				L. Pojoga, N. S. Kolatkar, J. S. Williams, T. S. Perlstein, X. Jeunemaitre, N. J. Brown, P. N. Hopkins, B. A. Raby, and G. H. Williams {beta}-2 Adrenergic Receptor Diplotype Defines a Subset of Salt-Sensitive Hypertension Hypertension, November 1, 2006; 48(5): 892 - 900. [Abstract] [Full Text] [PDF]

				N. S. Stachenfeld and H. S. Taylor Progesterone increases plasma volume independent of estradiol J Appl Physiol, June 1, 2005; 98(6): 1991 - 1997. [Abstract] [Full Text] [PDF]

				N. S. Stachenfeld, D. L. Keefe, and H. S. Taylor Responses to a Saline Load in Gonadotropin-Releasing Hormone Antagonist-Pretreated Premenopausal Women Receiving Progesterone or Estradiol-Progesterone Therapy J. Clin. Endocrinol. Metab., January 1, 2005; 90(1): 386 - 394. [Abstract] [Full Text] [PDF]

				N. S. Stachenfeld and H. S. Taylor Effects of estrogen and progesterone administration on extracellular fluid J Appl Physiol, March 1, 2004; 96(3): 1011 - 1018. [Abstract] [Full Text] [PDF]