Inhibitors of nitric oxide synthesis and ischemia/reperfusion attenuate coronary vasodilator response to pinacidil in isolated rat heart.

TL;DRAbstract

Evidence indicates that ATP-sensitive potassium channels (KATP) participate in the metabolic regulation of coronary flow and that this regulation is attenuated when endothelial production of nitric oxide (NO) is blocked. A hypothesis tested in this study was that, in hearts with the impaired NO-pathway, either with an inhibitor or as a result of ischemia/reperfusion, a coronary vasodilator response to KATP stimulation is impaired as well. In Langendorff perfused rat hearts, a blocker of NO synthesis (N omega-nitro-L-arginine, L-NOARG, 10 microM) and KATP inhibitor (glibenclamide, 0.6 microM) reduced the basal coronary flow by 44% and 29%, respectively. Glibenclamide caused a further 25% drop in the flow in L-NOARG perfused hearts. To determine the responsiveness of coronary resistance vessels to KATP stimulation and NO, dose-response curves (DRC) for KATP opener, pinacidil-, and NO-donor, 3-morpholino-syndomine-hydrochloride (SIN-1)-induced increase in coronary flow were constructed, r

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