Isolated rat hearts were perfused with a O
2--generating system consisting of purine plus xanthine oxidase for 15 or 20min. After the O
2- pretreatment, washout (performed with normal Krebs solution) produced significant elevation of coronary perfusion pressure (CPP). After 20min O
2- pretreatment, administration of 4μM nitroglycerin or 1μM sodium nitroprusside, which are nitric oxide (NO) donors, enhanced the elevation of CPP. Conversely, 100μM nitro-L-arginine or 10μM N
G-monomethyl-L-arginine, which are NO synthase inhibitors, immediately induced vasorelaxation in O
2--pretreated hearts. Thus, it was suggested that NO, a physiological vasodilator, paradoxically augments constriction of the coronary arteries, in O
2--pretreated rat heart.
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