cGMP-Dependent Protein Kinase Mediates NO- but not Acetylcholine-Induced Dilations in Resistance Vessels In Vivo
作者： Michael Koeppen , Robert Feil , Daniel Siegl , Susanne Feil , Franz Hofmann
DOI: 10.1161/01.HYP.0000147661.80059.CA
关键词:
摘要: cGMP and cGMP-dependent protein kinase type I (cGKI) mediate the dilation of large vessels in response to NO acetylcholine (ACh). However, physiological significance NO/cGMP/cGKI pathway resistance is controversial. Here, we analyzed NO- ACh-induced dilations arterioles cGKI-deficient (cGKI-/-) or endothelial synthase-deficient (eNOS-/-) mice. Mean arterial pressure was similar cGKI-/- wild-type mice (105 mm Hg). Pressure drops intracarotid bolus application donor sodium nitroprusside (SNP) were almost abolished mice, whereas decreases remained intact eNOS-/- The direct observation cremaster muscle by intravital microscopy showed impaired SNP-induced (by 80%) normal attenuated iberiotoxin 50%), indicating that they mediated part Ca2+-activated K+ channels, but not inhibitors cyclooxygenase p450-monooxygenases. We conclude cGKI are major effectors induce acute murine vessels. essential for basal blood regulation
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