Binding of aldosterone by mitochondria-rich cells of the toad urinary bladder

Abstract

ALDOSTERONE causes a large increase in the active transport of sodium by the urinary bladder1 of the toad. This response, analogous to the effects of the steroid on the kidney, has been the object of considerable biochemical study2. Aldosterone also enhances the stimulation by neurohypophyseal hormones of sodium and hydro-osmotic flux3,4. Because the response in sodium transport seems quantitatively related to the increment of cyclic AMP generated by vasopressin5, augmentation of the sodium response is presumably related to the larger increment of intracellular nucleotide induced by a given dose of vaso-pressin in steroid-treated bladders6. Using a technique for separating the two major cell types of the bladder mucosal epithelium—the granular (G) and the mitochondria-rich (MR) cells—we found that a response to neurohypophyseal hormones, as reflected by hormone-induced increases in the intracellular cyclic AMP content, is apparently limited to the MR cell7. This apparent synergism of the neurohypophyseal and steroid hormones on transport suggests that their loci of action are in close proximity. We therefore examined the binding of 3H-aldosterone by the two major cell types.