Integrative effects of nitric oxide and endothelium-derived hyperpolarizing factor induced by acetylcholine and bradykinin in rat hindquarter perfusion

We investigated the roles of endothelium-derived vasodilative factors in ra t hindquarter perfusion using a system for the direct measurement of nitric oxide (NO), Acetylcholine (ACh) induced the dose-dependent release of NO w ith a concomitant decrease in perfusion pressure. Under the influence of N- G-monomethyl-L-arginine (L-NMMA), NO release in response to ACh was blocked , while the perfusion pressure still decreased. In the presence of tetraeth ylammonium (TEA), the decrease in perfusion pressure in response to ACh was attenuated compared to the control value, The decrease in perfusion pressu re in response to ACh was almost abolished in the presence of both L-NMMA a nd TEA or with deendothelialization, Bradykinin (BI) also induced NO releas e and biphasic effects on the perfusion pressure. The perfusion pressure de creased with a lower concentration of BK and increased with a higher concen tration. L-NMMA and TEA each abolished the decrease in perfusion pressure i nduced by BK. Furthermore, in the presence of both L-NMMA and TEA, the perf usion pressure actually increased in response to BK. These results suggest that ACh and BE induce vasodilation through NO release and a potassium chan nel dependent mechanism via endothelium, (C) 2000 Academic Press.