Portal de Periódicos da CAPES

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

2000; Lippincott Williams & Wilkins; Volume: 87; Issue: 7 Linguagem: Inglês

10.1161/01.res.87.7.551

1524-4571

Kathy Loutzenhiser, Rodger Loutzenhiser,

Ion Transport and Channel Regulation

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