Angiotensin II–Induced Ca 2+ Influx in Renal Afferent and Efferent Arterioles

—Angiotensin II (Ang II)–induced Ca2+ signaling was studied in isolated rat renal arterioles using fura-2. Ang II (10 nmol/L) caused a sustained elevation in [Ca2+ ]i , which was dependent on [Ca2+ ]o in both vessel types. This response was blocked by nifedipine in only the afferent arteriole. Using the Mn2+ quench technique, we found that Ang II stimulates Ca2+ influx in both vessels. Nifedipine blocked the Ang II–induced Ca2+ influx in afferent arterioles but not in efferent arterioles. In contrast to Ang II, KCl-induced depolarization stimulated Ca2+ influx in only the afferent arteriole. Cyclopiazonic acid (CPA, 30 μmol/L) was used to examine the presence of store-operated Ca2+ entry in myocytes isolated from each arteriole. In efferent myocytes, CPA induced a sustained Ca2+ increase that was dependent on [Ca2+ ]o and insensitive to nifedipine. This mechanism was absent in afferent myocytes. SKF 96365 inhibited Ang II–induced Ca2+ entry in efferent arterioles and CPA-induced Ca2+ entry in efferent myocytes over identical concentrations. Our findings thus indicate that Ang II activates differing Ca2+ influx mechanisms in pre- and postglomerular arterioles. In the afferent arteriole, Ang II activates dihydropyridine-sensitive L-type Ca2+ channels, presumably by membrane depolarization. In the efferent arteriole, Ang II appears to stimulate Ca2+ entry via store-operated Ca2+ influx.