Evidence for the presence in arterial walls of intracellular-molecular mechanism for action of mineralocorticoids.

Abstract

Data from clinical and experimental studies indicate that mechanism(s) for action of mineralocorticoids, other than renal, must be involved in the overall effect of mineralocorticoids on circulation--increased peripheral resistance and hypertension. We have postulated existence of such a mechanism in the arterial wall and have looked for the evidence for its presence. We have found high affinity, specific binders for mineralocorticoids, and glucocorticoids, with characteristics of steroid receptors, in the cytosol of rabbit aorta and femoral and carotid arteries. These binders possess physicochemical properties of steroid receptors and, moreover, they translocate to cell nuclei (as steroid-receptor complexes) and bind to relatively specific "acceptor-sites" on nuclear chromatin. This provides evidence for the existence of an intracellular-molecular mechanism for a direct in situ action of mineralocorticoids, and also glucocorticoids, in the arterial wall. We postulate that the demonstrated previously effect of mineralocorticoids on arterial smooth muscle cell-membrane permeability to electrolytes, leading presumably to increased peripheral resistance and hypertension, is elicited through the receptor-mediated mechanism for action of mineralocorticoids in the arterial wall.