Alpha 2 adrenoreceptors are located on vascular smooth muscle of the rat tail artery. In the present study this receptor was studied in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. Adrenergic agonists were used to produce isometric contractions of helically-cut tail artery strips from SHR and WKY. Clonidine and guanabenz, alpha 2 agonists, were more potent in the SHR than in the WKY (e.g. clonidine: EC50 SHR = 3.5 +/- 0.6 X 10(-8) M; EC50 WKY = 17.0 +/- 0.2 X 10(-8) M; P less than 0.0005). There was no difference in potency between the alpha 1 agonists, phenylephrine and methoxamine. Yohimbine, an alpha 2 antagonist, was more potent in inhibiting the clonidine-induced contraction in the SHR (pA2 = 7.66 versus 7.14). To determine the number of alpha 2 adrenoreceptors, the specific binding of 3H-clonidine to homogenates of tail artery and of five brain areas was also measured. The maximum number of high-affinity sites on the tail artery was threefold greater in SHR than in WKY (31 +/- 5 versus 11 +/- 3 fmol/mg protein, P less than 0.0005). No differences in the number or affinity of alpha 2 receptor sites was found in the hypothalamus, hippocampus, locus coeruleus or parietal cortex of the two strains of rat. There was a difference in the amygdala (SHR: 163 +/- 16 versus WKY: 108 +/- 14, P less than 0.05). The larger number of alpha 2 adrenoreceptors on the vascular smooth muscle in SHR may provide an explanation for the supersensitivity of SHR to adrenergic agonists.
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WEISS et al. (1984) studied this question.