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 flux^3,4. 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.