Evidence of bPTH-(1-34) sensitive adenylate cyclase in isolated rabbit renal cortex arterioles.

Abstract

Current evidence suggest that parathyroid hormone (PTH), regulates Ca homeostasis by activating kidney and bone adenylate cyclase. In addition to this action, PTH has physiological effects, on the cardiovascular system. The synthetic 1-34 fragment of bovine PTH shows direct hypotensive action in the anesthetized dog (1). Extracted and synthetic PTH increases the arterial blood flow of renal and hepatic arteries (2). It has also been reported that PTH relaxes rat aortic strip in vitro to a slight but significant degree (3) and that para thyroid extract acts on arterial blood pressure, contraction and 45Ca exchange in isolated rat aorta (4). The question that arises is whether or not PTH affects adenylate cyclase activity of isolated vascular and microvascular beds. It has also been just reported that bPTH-(1-34) stimulates adenylate cyclase in rat cerebral microvessels in much the same way as in the renal cortex (5). In a recent work (6) we described a successful method for isolating rabbit renal cortical and preglomerular arterioles characterized by their high renin content and the enrichment of the muscle-specific enzyme creatin-kinase. The present work examined the possible effect of bPTH-(1-34) on adenylate cyclase of such microvessels which play an important role in the renal and peripheral hemodynamic and glomerulo-tubular feed-back control.