Lack of NO formation is involved in the vasodilative response to contrast media

Abstract

Intravascular injection of angiographic contrast media results in peripheral vasodilation and hypotension. The mechanisms underlying these hemodynamic changes are not entirely clear. We hypothesized that increased formation of nitric oxide (NO) could be involved in the vasodilatory response to contrast media. To address this assumption we have investigated whether N^G-monomethyl-L-arginine (L-NMMA, 200 mg/kg) and N^G-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg), two specific NO formation inhibitors, can abolish the hypotensive response to intravascular injection of isopaque amin (1 g/kg), a contrast medium, as well as bradykinin (10 μg/kg), a NO-dependent vasodilator, in anaesthetized normotensive rats. In rats before pretreatment with L-NMMA and L-NAME, the absolute values of the average fall in mean arterial pressure (MAP) induced by intravascular injection of isopaque amin and bradykinin were 21.3 ± 2.1 and 37.2 ± 4.4 mmHg, respectively. Pretreatment with L-NMMA and L-NAME failed to affect the hypotensive response to isopaque amin; by administering isopaque amin in rats pretreated with L-NMMA and L-NAME the absolute values of the average fall in MAP were 25.6 ± 4.9 and 23.4 ± 3.9 mmHg, respectively, similar to the average fall in MAP before treatment with NO formation inhibitors. In contrast, the hypotensive response to bradykinin was significantly inhibited; by administering bradykinin in rats pretreated by L-NMMA and L-NAME, the absolute values of the average fall in MAP were 10.2 ± 2.8 and 7.2 ± 2.2 mmHg, respectively, much less than the average fall in MAP before treatment with NO formation inhibitors. We conclude that intravascular injection of isopaque amin causes reduction in systemic arterial pressure. However, this vasodilative effect seems unrelated majorly to augmented endothelium-derived NO formation.