作者: Guo Hua Liang , Qi Xi , Charles W. Leffler , Jonathan H. Jaggar
DOI: 10.1113/JPHYSIOL.2011.225128
关键词:
摘要: Hydrogen sulfide (H2S) is a gaseous vasodilator produced by endothelial cells. Mechanisms which H2S induces vasodilatation are unclear. We tested the hypothesis that dilates cerebral arterioles modulating local and global intracellular Ca2+ signals in smooth muscle High-speed confocal imaging revealed Na2S, an donor, increased spark frequency ∼1.43-fold decreased concentration ([Ca2+]i) ∼37 nm cells of intact piglet arterioles. In contrast, did not alter wave frequency. voltage-clamped (−40 mV) cells, iberiotoxin-sensitive, spark-induced transient Ca2+-activated K+ (KCa) currents ∼1.83-fold, but amplitude these events. activity single KCa channels recorded absence sparks arteriole SR load ([Ca2+]SR), measured as caffeine (10 20 mm)-induced [Ca2+]i transients, ∼1.5-fold. hyperpolarized (by ∼18 dilated pressurized (40 mmHg) Iberiotoxin, channel blocker, reduced H2S-induced hyperpolarization ∼51%. Iberiotoxin ryanodine, ryanodine receptor inhibitor, ∼38 ∼37%, respectively. summary, our data indicate elevates [Ca2+]SR, leading to activation The subsequent elevation current leads membrane hyperpolarization, reduction vasodilatation.