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1 Ion Channel and Calcium Signaling Unit/Molecular Medicine, Boston University School of Medicine, Boston, Massachusetts, United States
2 Vascular Biology Unit/Medicine, Boston University School of Medicine, Boston, Massachusetts, United States
* To whom correspondence should be addressed. E-mail: bolotina{at}bu.edu.
Store-operated channels (SOC) and Ca2+ entry (SOCE) 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, as voltage-gated L-type Ca2+ channels (Ca2+L) are thought to be fully responsible for agonist-induced Ca2+ influx and vasoconstriction. Here we present evidence that SOC channels and their activation via a Ca2+-independent phospholipase A2 (iPLA2)-mediated pathway plays a crucial role in agonist-induced constriction of cerebral, mesenteric and carotid arteries. Intracellular Ca2+ in SMC and intraluminal diameter were measured simultaneously in intact pressurized vessels in vitro. We demonstrated that: 1) Ca2+ and contractile responses to phenylephrine (PE) in cerebral and carotid arteries were equally abolished by nimodipine (Nim, Ca2+Linhibitor), and by 2-aminoethyl diphenylborinate (2-APB, inhibitor of SOC), suggesting that SOC and Ca2+Lboth may be involved in agonist-induced constriction of cerebral arteries; 2) functional inhibition of iPLA2
totally inhibited PE-induced Ca2+ influx and constriction in cerebral, mesenteric and carotid arteries, while K+-induced Ca2+ influx and vasoconstriction mediated by Ca2+L channels remained intact. Thus, iPLA2-dependent activation of SOC channels is crucial for agonist-induced Ca2+ influx and vasoconstriction in cerebral, mesenteric and carotid arteries. We propose that upon PE-induced depletion of Ca2+ stores, nonselective SOC channels are activated via iPLA2-dependent pathway, and may produce depolarization of SMC that could trigger a secondary activation of Ca2+L channels, which lead to Ca2+ entry and vasoconstriction
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