Cooling effects on the histaminergic response of rabbit ear and femoral arteries: role of the endothelium

Publisher Website
Google Scholar
Abstract
The effects of cooling on the isometric response of rabbit isolated central ear (cutaneous) and femoral (non‐cutaneous) arteries to histamine were determined at 37oC and 24oC (cooling). Under resting tension, both types of arteries contracted to histamine (10‐7‐10‐3M), and the sensitivity of ear arteries, but not of femoral arteries was lower at 24 than at 37oC. Chlorpheniramine (10‐7M) blocked the contraction of both types of arteries to histamine at both temperatures. In ear arteries, endothelium removal or treatment with the nitric oxide synthase inhibitorNG‐nitro‐L‐arginine methyl ester (L‐NAME, 10‐5M) did not affect the contraction to histamine at 37oC, but it reversed the decreased contraction at 24oC. In femoral arteries, endothelium removal or L‐NAME (10‐5M) did not affect the response to histamine at 37 and 24oC. Ear and femoral arteries precontracted with endothelin‐1 (10‐8‐10‐7M) and pretreated with chlorpheniramine (10‐5M) relaxed to histamine (10‐7‐10‐4M), and the sensitivity of this relaxation in ear arteries, but not in femoral arteries, increased at 24oC. The relaxation of ear and femoral arteries to histamine was not modified by endothelium removal, L‐NAME (10‐5M) or meclofenamate (10‐5M), but it was blocked by cimetidine (10‐6M) at 37oC and 24oC. These results suggest: (1) ear and femoral arteries have contracting H1and relaxing H2receptors, probably located on smooth musculature, and (2) cooling reduces the contraction and increases the relaxation of cutaneous arteries to histamine: the reduction of this contraction could be caused by an augmented availability of endothelial nitric oxide, and the increment of this relaxation could be caused by an augmented sensitivity of H2receptors of smooth musculature induced by cooling. These features do not seem to occur in deep vessels.