In cutaneous veins of the dog, cooling augments the response to sympathetic nerve stimulation and exogenous norepinephrine (NE). The postjunctional α adrenoceptors in this blood vessel belong to both the α1 and α2 subtypes. Cooling augments α2-adrenergic responses (presumably because of an increased receptor affinity), but depresses α1-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 α1 adrenoceptor reserve is present that buffers the response from the inhibitory effect of cooling. This allows the potentiating effect of cold on the α2-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 α1- and α2-adrenergic activation. This can be explained best by the absence of a receptor reserve for α1-adrenergic agonists of high efficacy, combined with a reduced density of postjunctional α2 adrenoceptors.
|Original language||English (US)|
|Number of pages||8|
|State||Published - Jan 1 1986|
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