Mechanisms underlying endothelium-dependent flow increase in perfused rat mesenteric vascular bed. 
The isolated rat mesenteric vasculature was perfused at constant pressures of 40, 80 or 120 mm Hg and the change in flow rate was measured.  In the presence of phenylephrine, treatment with 3-[(3-cholamidopropyl) dimethylammonio]-1-propane sulfonate (CHAPS) or N(G)-nitro-L-arginine (L-NA) significantly inhibited the pressure-dependent flow rate increase, but treatment with indomethacin or charybdotoxin plus apamin did not.  Acetylcholine, bradykinin and ADP increased the flow rate, which had been markedly suppressed by CHAPS.  At 80 mm Hg, the flow rate increase induced by these agonists was not affected by indomethacin plus L-NA, but was suppressed by subsequent treatment with charybdotoxin plus apamin.  Changes in the perfusion pressure did not significantly affect the flow rate increases induced by the agonists.  In conclusion, the opening of charybdotoxin plus apamin-sensitive Ca(2+)-dependent K(+) channels may be mainly involved in the endothelium-dependent flow rate increase induced by the agonists, whereas nitric oxide (NO) may be responsible for the endothelium-dependent, pressure-induced flow rate increase.