Angiotensin II-induced Ca2+ influx in renal afferent and efferent arterioles - Differing roles of voltage-gated and store-operated Ca2+ entry

Angiotensin II (Ang LI)-induced Ca2+ signaling was studied in isolated rat renal arterioles using fura-2. Ang II (10 nmol/L) caused a sustained elevat ion in [Ca2+](i), which was dependent on [Ca2+](o) in both vessel types. Th is 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-indu ced depolarization stimulated Ca2+ influx in only the afferent arteriole. C yclopiazonic acid (CPA, 30 mu mol/L) was used to examine the presence of st ore-operated Ca2+ entry in myocytes isolated from each arteriole. In effere nt myocytes, CPA induced;a sustained Ca2+ increase that was dependent on [C a2+](o) and insensitive to nifedipine. This-mechanism was absent in afferen t myocytes. SKF 96365 inhibited Ang II-induced Ca2+ entry in efferent arter ioles and CPA-induced Ca2+ entry in efferent myocytes over identical concen trations. Our findings thus indicate that Ang II activates differing Ca2+ i nflux mechanisms in pre- and postglomerular arterioles. In the afferent art eriole, Ang II activates dihydropyridine-sensitive L-type Ca2+ channels, pr esumably by membrane depolarization. In the efferent arteriole, Ang II appe ars to stimulate Ca2+ entry via store-operated Ca2+ influx.