Functional Adrenocorticotropic Hormone Receptor in Cultured Human Vascular Endothelial Cells

Author:

Hatakeyama Haruhiko1,Inaba Satoru1,Taniguchi Naomi1,Miyamori Isamu1

Affiliation:

1. From the Third Department of Internal Medicine, Fukui Medical University, Fukui, Japan.

Abstract

Abstract —Hypertension is a prominent feature of patients with Cushing’s disease and ectopic adrenocorticotropic hormone (ACTH) syndrome, who have elevated ACTH levels. Chronic administration of ACTH (1-24) also raises blood pressure in humans. This effect has been postulated to be due to ACTH-induced increases in cortisol secretion in the adrenal gland. It is well known that cortisol increases vascular tone by potentiating the vasoconstrictor action of a number of pressor hormones. In the present study, we show direct evidence that human aortic endothelial cells possess the ACTH receptor. 11β-Dehydrogenation, converting cortisol to its inactive metabolite, cortisone, mediated by vascular 11β-hydroxysteroid dehydrogenase type 2 is essential for the control of vascular tone, and the reduced activity may be relevant to the pathogenesis of hypertension. We found that ACTH (1-24) dose-dependently decreased the gene expression and enzyme activity of 11β-hydroxysteroid dehydrogenase type 2 in these cells, and the decrease was partially abolished by a selective ACTH receptor antagonist. This may indicate that ACTH potentiates the action of cortisol through its direct effect on the vasculature. Therefore, the present study provides important information for understanding the mechanism of ACTH-induced hypertension.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Internal Medicine

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