Vanhoutte P M, Flavahan N A
Fed Proc. 1986 Aug;45(9):2347-54.
In cutaneous veins of the dog, cooling augments the response to sympathetic nerve stimulation and exogenous norepinephrine (NE). The postjunctional alpha adrenoceptors in this blood vessel belong to both the alpha 1 and alpha 2 subtypes. Cooling augments alpha 2-adrenergic responses (presumably because of an increased receptor affinity), but depresses alpha 1-adrenergic responses (presumably because of a direct inhibitory effect on the contractile process). When agonists of high efficacy such as NE or phenylephrine are used, an alpha 1-adrenoceptor reserve is present that buffers the response from the inhibitory effect of cooling. This allows the potentiating effect of cold on the alpha 2-adrenergic component of the response to catecholamines to predominate, and the contractile response to exogenous NE and sympathetic nerve stimulation is augmented. By contrast, in deep veins of the limb, cold reduces the contractions evoked by alpha 1- and alpha 2-adrenergic activation. This can be explained best by the absence of a receptor reserve for alpha 1-adrenergic agonists of high efficacy, combined with a reduced density of postjunctional alpha 2 adrenoceptors.
在犬的皮肤静脉中,降温可增强对交感神经刺激和外源性去甲肾上腺素(NE)的反应。该血管中的节后α肾上腺素能受体属于α1和α2两种亚型。降温可增强α2肾上腺素能反应(可能是由于受体亲和力增加),但会抑制α1肾上腺素能反应(可能是由于对收缩过程有直接抑制作用)。当使用高效能激动剂如NE或去氧肾上腺素时,存在α1肾上腺素能受体储备,可缓冲降温的抑制作用对反应的影响。这使得寒冷对儿茶酚胺反应中α2肾上腺素能成分的增强作用占主导,对外源性NE和交感神经刺激的收缩反应增强。相比之下,在肢体的深部静脉中,寒冷会减弱由α1和α2肾上腺素能激活所诱发的收缩。这可以通过缺乏对高效能α1肾上腺素能激动剂的受体储备,以及节后α2肾上腺素能受体密度降低来最好地解释。