Role of the endothelium in the response to cholinoceptor stimulation of rabbit ear and femoral arteries during cooling.

1. The role of the endothelium in the effects of cooling on the response to cholinoceptor stimulation of the rabbit central ear (cutaneous) and femoral (non-cutaneous) arteries was studied using 2 mm long cylindrical segments. 2. Concentration-response curves for acetylcholine (10(-9)-10(-5) M), methacholine (10(-9)-10(-5) M) and sodium nitroprusside (10(-9)-10(-4) M) were isometrically recorded in arteries under conditions, with and without endothelium or following pretreatment with the nitric oxide-synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 10(-6)-3 x 10(-4) M) at 37 degrees C and at 24 degrees C (cooling). 3. Ear and femoral arteries showed endothelium-dependent relaxation to acetylcholine and methacholine at 37 degrees C and 24 degrees C. The extent of relaxation of the control ear arteries, but not of the control femoral arteries, to acetylcholine and methacholine increased during cooling. 4. L-NAME (10(-6)-3 x 10(-4) M) reduced in a concentration-dependent way the response of ear arteries to acetylcholine at both 37 degrees C and 24 degrees C, this reduction being more potent at 37 degrees C. L-Arginine (10(-5)-10(-3) M) reversed in a concentration-dependent manner the inhibitor effects of 10(-5) M L-NAME at both temperatures. 5. Sodium nitroprusside caused a concentration-dependent relaxation in both arteries that was endothelium-independent. However, the extent of relaxation to this nitrovasodilator in ear and femoral arteries was lower at 24 degrees C. 6. These results suggest that cooling augments the reactivity of cutaneous (ear) arteries, but not that of non-cutaneous (femoral) arteries to cholinoceptor stimulation by endothelium-mediated mechanisms.Cooling could therefore facilitate the stimulated release of endothelial nitric oxide in cutaneous vessels.