Cooling and response to adrenoceptor agonists of rabbit ear and femoral artery: role of the endothelium

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Abstract
1 The effects of cooling on the response of the rabbit central ear (cutaneous) and femoral (non-cutaneous) arteries to stimulation of adrenoceptors and the role of the endothelium in these effects, were studied in 2 mm long cylindrical segments. 2 Concentration-response curves for noradrenaline (10−9 − 3 × 10−4 m), phenylephrine (α1-adrenoceptor agonist, 10−9 − 3 × 10−4 m) and B-HT 920 (α2-adrenoceptor agonist, 10−7 − 10−3 m) were recorded isometrically in arteries with and without endothelium at 37°C and at 24°C (cooling). To analyze further the endothelial mechanisms in the responses to adrenoceptor stimulation during cooling, the effects of the adrenoceptor agonists on ear arteries in the presence of NG-nitro-l-arginine methyl esther (l-NAME) (10−5 m) were also determined. 3 In every condition tested, the three adrenoceptor agonists produced a concentration-dependent arterial contraction and the order of potency in ear and femoral arteries was noradrenaline ≥ phenylephrine > B-HT 920. The response of ear and femoral arteries to phenylephrine or B-HT 920 was blocked by prazosin (10−6 m). Yohimbine (10−6 m) decreased slightly the response of ear arteries and increased that of femoral arteries to B-HT 920. 4 The sensitivity of both ear and femoral arteries to the three adrenoceptor agonists was significantly lower at 24°C than at 37°C. 5 In ear arteries, endothelium removal or treatment with l-NAME did not influence the response at 37°C, but did increase it during cooling to adrenoceptor stimulation. In femoral arteries, endothelium removal increased the sensitivity to noradrenaline and, especially, to B-HT 920 at 37°C, but did not affect the response at 24°C. 6 The results suggest that: (a) rabbit ear and femoral arteries are equipped mainly with α1-adrenoceptors; (b) at 37°C, the contraction of the ear artery to adrenoceptor agonists is mostly endothelium-independent, and in the femoral artery the contraction to α2-adrenoceptor activation is endothelium-dependent; (c) cooling inhibits the contraction to adrenoceptor agonists in both ear and femoral arteries: in the ear artery probably by increasing the availability of endothelial nitric oxide, but in the femoral artery by depressing the sensitivity of α-adrenoceptors in the smooth musculature. 7 The results suggest that the endothelium may modulate the adrenoceptor response of cutaneous arteries during changes in temperature.