Role of nitric oxide in rat coronary flow regulation during respiratory and metabolic acidosis.
A rat Langendorff heart preparation, perfused at constant pressure, was used to evaluate the role of nitric oxide in the increases in coronary vessel flow during hypercapnic and metabolic acidosis. Prior administration of the nitric oxide synthase (NOS) inhibitor N6-nitro-L-arginine methyl ester (100 microM) significantly reduced the basal, resting, rate of coronary flow but did not attenuate the increases in flow during brief (2-min) periods of perfusion with acidotic solutions. These results suggest that nitric oxide is not a significant contributor to rat heart coronary flow regulation during respiratory or metabolic acidosis.
Song
D
D
Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.
O'Regan
M H
MH
Phillis
J W
JW
D000138:Acidosis / Q000139:chemically induced / Q000201:enzymology / Q000503:physiopathology*; D000818:Animals; D001783:Blood Flow Velocity / Q000187:drug effects; D003326:Coronary Circulation / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006935:Hypercapnia; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D051381:Rats; D017207:Rats, Sprague-Dawley; D014664:Vasodilation / Q000187:drug effects
D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester