A rat Langendorff heart preparation, perfused at constant pressure, was use
d 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 N-6-nitro-L-arginine methyl ester (1
00 mu M) significantly reduced the basal, resting, rate of coronary flow bu
t did not attenuate the increases in flow during brief (2-min) periods of p
erfusion with acidotic solutions. These results suggest that nitric oxide i
s not a significant contributor to rat heart coronary flow regulation durin
g respiratory or metabolic acidosis. (C) 1999 Elsevier Science Inc. All rig
hts reserved.