Angiotensin II-induced changes in smooth muscle calcium in rat renal arterioles.

Abstract

The isolated rat renal arteriole technique was adapted for use in a fluorescence ratio imaging system in which angiotensin II (AII)-induced changes in lumen diameter and smooth muscle cell (SMC) cytosolic calcium [(Ca2+]i were serially determined for 4 min with Fura-2. Selective fluorescence acquisition from SMC was guided by direct image visualization of the vessel walls. A maximal constricting concentration of AII (10(-8) M) caused similar abrupt and sustained increases in SMC [Ca2+]i in afferent arterioles (AA) at 80 mm Hg and efferent arterioles (EA) at 30 mm Hg. When lumen pressure was reduced to 0 mm Hg, 10(-8) M AII caused abrupt peak increases in SMC [Ca2+]i in 15 s in both AA and EA, which declined rapidly thereafter--patterns distinctly different from pressurized vessels (P < 0.02). With diltiazem (10(-5) M) in the bathing media, 10(-8) M AII caused an abrupt rise and decline in SMC [Ca2+]i in AA, but a sustained elevation in EA (P < 0.02). In low-Ca(2+)-EGTA media, there was an abrupt peak and rapid decline in SMC [Ca2+]i to 10(-8) M AII in AA and EA; the abrupt peaks were attenuated by the prior addition of dantrolene (5 x 10(-5) M) to the low-Ca(2+)-EGTA media. When half-maximal constricting (EC50) AII for AA (4 x 10(-11) M) was added, there was a slow, progressive increase in SMC [Ca2+]i that was distinctly different from the abrupt peak and decline with EC50 AII (5 x 10(-12) M) in EA. Collectively, these findings indicate that maximal AII stimulates both Ca2+ entry and storage mobilization in AA and EA; EC50 AII stimulates primarily Ca2+ entry in AA, but storage mobilization in EA. Lumen pressure modifies the AII SMC [Ca2+]i response profiles.