DISRUPTION OF THE RAT MESENTERIC ARTERIAL BED ENDOTHELIAL FUNCTION BYAIR PERFUSION

The impact of air perfusion on the endothelial function of the rat mes enteric arterial bed (MAB; perfused with Krebs' bicarbonate plus indom ethacin) was compared to that of the NO synthase inhibitor, N-omega-ni tro-L-arginine methyl ester (L-NAME). Air shifted the dose-response cu rve for the alpha-adrenoceptor agonist, norepinephrine (NE) to the lef t (ED50%: 2.9+/-0.7 to 0.9+/-0.7 mu g, P < 0.05); maximal vasoconstric tion did not change. L-NAME produced a similar increase in midrange se nsitivity (ED50, 1.4+/-0.7 mu g, P < 0.05) and a 20% increase in maxim um (152+/-6 to 183+/-7 mmHg, P < 0.05). Electromechanical stimulation with potassium chloride (KCl) was not modified by reserpine. Neither a ir nor L-NAME modified midrange sensitivity to KCI. L-NAME produced a 17% increase in maximum (91+/-4 to 107+/-5 mmHg, P < 0.05); reserpine abolished the latter effect. Air and L-NAME diminished endothelium-dep endent vasodilation elicited by carbachol. Air did not modify endothel ium-dependent vasodilation elicited by sodium nitroprusside; this resp onse was potentiated by L-NAME. In summary, air and L-NAME produced si milar effects on receptor-dependent activation of the endothelial L-ar ginine nitric oxide (NO) pathway. Potentiation by L-NAME of the maxima l electromechanical response suggests the existence of a tone-dependen t NO system. Abolition of the latter response by reserpine suggests th at this system is of sympathetic origin.