Halothane inhibition of acetylcholine-induced relaxation in rat mesenteric artery and aorta

The effect of halothane was compared on acetylcholine (ACh)-induced relaxation of the mesenteric artery and the aorta in rats.

The responses of isolated rat aortic and mesenteric arterial ring segments precontracted with phenylephrine to ACh (10(-8)-10(-5) M), in the presence of halothane 0-3%, were compared using isometric force tension recordings. Effects of NG-nitro-l-arginine (L-NOARG, 3 x 10(-5), methylene blue (MB, 5 x 10(-6) M), oxyhaemoglobin in (OxyHB, 10(-7) M), and various potassium channel inhibitors; tetraethylammonium (TEA, 10(-5) M, 10(-3) M), apamin (AP, 10(-7) M), charybdotoxin (ChTx, 10(-7) M) and glibenclamide (GC, 10(-5) M) on ACh-induced relaxation in mesenteric artery were tested. Using radioimmunoassay, ACh (10(-6) M)-induced guanosine 3':5'-cyclic monophosphate (cGMP) accumulation of mesenteric arterial rings pretreated with L-NAORG were also measured.

L-NOARG partially inhibited ACh-induced relaxation in mesenteric arterial rings (P < 0.05, maximum relaxation reduced by approximately 50%), whereas it abolished them in aortic rings. The remaining relaxation resistant to L-NOARG in mesenteric arterial rings was insensitive to additional MB or OxyHB, and was not accompanied by increases in cGMP contents of rings. Halothane inhibited endothelium-dependent relaxation in aorta and mesenteric arterial rings. This inhibitory effect was larger in aorta. Halothane also inhibited NO independent EDHF-dependent relaxation in the mesenteric arterial rings,

Despite a similar inhibitory effect on the EDHF relaxing pathway, halothane has a larger effect on endothelium-dependent relaxation in the aorta (NO dependent mainly) than in the mesenteric rings (NO and EDHF dependent).