Disruption of the rat mesenteric arterial bed endothelial function by air perfusion

The impact of air perfusion on the endothelial function of the rat mesenteric arterial bed (MAB; perfused with Krebs' bicarbonate plus indomethacin) was compared to that of the NO synthase inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME). Air shifted the dose-response curve for the alpha-adrenoceptor agonist, norepinephrine (NE) to the left (ED50%: 2.9+/-0.7 to 0.9+/-0.7 microg, P < 0.05); maximal vasoconstriction did not change. L-NAME produced a similar increase in midrange sensitivity (ED50% 1.4+/-0.7 microg, P < 0.05) and a 20% increase in maximum (152+/-6 to 183+/-7 mmHg, P < 0.05). Electromechanical stimulation with potassium chloride (KCl) was not modified by reserpine. Neither air nor L-NAME modified midrange sensitivity to KCl. 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-dependent vasodilation elicited by carbachol. Air did not modify endothelium-dependent vasodilation elicited by sodium nitroprusside; this response was potentiated by L-NAME. In summary, air and L-NAME produced similar effects on receptor-dependent activation of the endothelial L-arginine nitric oxide (NO) pathway. Potentiation by L-NAME of the maximal electromechanical response suggests the existence of a tone-dependent NO system. Abolition of the latter response by reserpine suggests that this system is of sympathetic origin.