The role of nitric oxide in the regulation of coronary flow and mechanical function of isolated, perfused rat hearts.
The role of nitric oxide (NO) in the regulation of coronary flow and mechanical function under basal conditions and when exposed to nifedipine was studied in perfused rat hearts. Inhibition of basal release of NO by bolus injections of NG-nitro-L-arginine (L-NNA) (90 mM) and NG-nitro-L-arginine methyl ester (L-NAME) (185, 370 and 740 mM) induced significant decrease in coronary flow, contractile force and heart rate. L-NAME in the doses of 185, 370 and 740 mM also decreased significantly contractile force and heart rate during treatment with 170 microM nifedipine. However, the same doses of L-NAME caused an insignificant reduction in coronary flow in the presence of nifedipine. These findings suggest that NO has an important role in the regulation of coronary flow and mechanical performance under basal conditions and during the hearts exposed to nifedipine. Nifedipine may attenuate the myocardial ischaemia induced by the loss of NO production.
Department of Physiology, Faculty of Medicine, University of Osmangazi, Eskişehir, Türkiye.
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D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000008:administration & dosage; D005260:Female; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D019331:NG-Nitroarginine Methyl Ester / Q000008:administration & dosage; D009543:Nifedipine / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D019335:Nitroarginine / Q000008:administration & dosage; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar
D004791:Enzyme Inhibitors; D019335:Nitroarginine; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D009543:Nifedipine; D019331:NG-Nitroarginine Methyl Ester