Analysis of angiotensin-stimulated sodium transport in cultured smooth muscle cells from rat aorta

✍ Scribed by Jeffrey Bingham Smith; Tommy A. Brock

• Publisher: John Wiley and Sons
• Year: 1983
• Tongue: English
• Weight: 884 KB
• Volume: 114
• Category: Article
• ISSN: 0021-9541
• DOI: 10.1002/jcp.1041140306

✦ Synopsis

Angiotensin peptides (Al, All, Alll) increased the rate of Na+ accumulation by smooth muscle cells (SMC) cultured from rat aorta. The stimulatory effect of All on Na+ uptake was observed when N a + exodus via the Na+/K+ pump was blocked either by ouabain or by the removal of extracellular K + . All was at least ten times more potent than All1 and about 100 times more potent than Al in stimulating Na+ uptake. Saralasin had little effect on Na+ uptake by itself but almost completely blocked the increase caused by All. The stimulation of net Na+ entry by Al, but not All, was prevented by protease inhibitors. The stimulation of Na+ uptake was almost completely blocked by amiloride. Tetrodotoxin, which prevented veratridine from increasing Na+ uptake, had no effect on the response to All. Angiotensin increased the rate of ouabainsensitive 86Rb+ uptake (Na+/K+ pump activity) but had no effect on ouabainsensitive ATPase activity in frozen-thawed SMC or in microsomal membranes isolated from cultured SMC. The stimulation of ouabain-sensitive "Rb+ uptake by All was blocked by saralasin. Omitting Na+ from the external medium prevented All from increasing "Rb+ uptake. All had no effect on cell volume or cyclic AMP levels in the cultured SMC. These results suggest that angiotensin peptides activate an amiloride-sensitive Na+ transporter which supplies the Na+/K+ pump with more Na+, its rate-limiting substrate.