Back to Search
Start Over
Role of [iPLA.sub.2] and store-operated channels in agonist-induced [Ca.sup.2+] influx and constriction in cerebral, mesenteric, and carotid arteries
- Source :
- The American Journal of Physiology. March, 2008, Vol. 294 Issue 3, pH1183, 5 p.
- Publication Year :
- 2008
-
Abstract
- Store-operated channels (SOC) and store-operated [Ca.sup.2+] entry are known to play a major role in agonist-induced constriction of smooth muscle cells (SMC) in conduit vessels. In microvessels the role of SOC remains uncertain, in as much as voltage-gated L-type [Ca.sup.2+] ([Ca.sup.2+.sub.L]) channels are thought to be fully responsible for agonist-induced [Ca.sup.2+] influx and vasoconstriction. We present evidence that SOC and their activation via a [Ca.sup.2+] -independent phospholipase [A.sub.2] ([iPLA.sub.2])-mediated pathway play a crucial role in agonist-induced constriction of cerebral, mesenteric, and carotid arteries. Intracellular [Ca.sup.2+] in SMC and intraluminal diameter were measured simultaneously in intact pressurized vessels in vitro. We demonstrated that 1) [Ca.sup.2+] and contractile responses to phenylephrine (PE) in cerebral and carotid arteries were equally abolished by nimodipine (a [Ca.sup.2.sub.L+] inhibitor) and 2-aminoethyl diphenylborinate (an inhibitor of SOC), suggesting that SOC and [Ca.sup.2.sub.L+] channels may be involved in agonist-induced constriction of cerebral arteries, and 2) functional inhibition of [iPLA.sub.2][beta] totally inhibited PE-induced [Ca.sup.2+] influx and constriction in cerebral, mesenteric, and carotid arteries, whereas [K.sup.+]-induced [Ca.sup.2+] influx and vasoconstriction mediated by [Ca.sup.2+.sub.L] channels were not affected. Thus [iPLA.sub.2]-dependent activation of SOC is crucial for agonist-induced [Ca.sup.2+] influx and vasoconstriction in cerebral, mesenteric, and carotid arteries. We propose that, on PE-induced depletion of [Ca.sup.2+] stores, nonselective SOC are activated via an [iPLA.sub.2]-dependent pathway and may produce a depolarization of SMC, which could trigger a secondary activation of [Ca.sup.2+.sub.L] channels and lead to [Ca.sup.2+] entry and vasoconstriction. store-operated calcium entry; smooth muscle cells; constriction
- Subjects :
- Vasoconstriction -- Evaluation
Muscle cells -- Properties
Vascular endothelium -- Properties
Ion channels -- Evaluation
Phospholipases -- Physiological aspects
Cerebral arteries -- Health aspects
Cerebral arteries -- Properties
Carotid artery -- Health aspects
Carotid artery -- Properties
Calcium channels -- Health aspects
Calcium channels -- Properties
Biological sciences
Subjects
Details
- Language :
- English
- ISSN :
- 00029513
- Volume :
- 294
- Issue :
- 3
- Database :
- Gale General OneFile
- Journal :
- The American Journal of Physiology
- Publication Type :
- Academic Journal
- Accession number :
- edsgcl.177265956