Affiliation:
1. From the Smooth Muscle Research Group, Department of Pharmacology and Therapeutics, University of Calgary, Alberta, Canada.
Abstract
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.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Cardiology and Cardiovascular Medicine,Physiology
Cited by
111 articles.
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