Postsynaptic alpha-adrenoceptor subtypes in the internal carotid, mesenteric, splenic, renal and femoral vascular beds of the dog.

Pressor effects of noradrenaline, phenylephrine and alpha-methylnoradrenaline and the inhibition of these effects by prazosin or yohimbine (or both) were studied in vivo in the renal, splenic, femoral, anterior mesenteric and internal carotid vascular beds of the dog. In all the vascular beds noradrenaline was more potent than alpha-methylnoradrenaline and alpha-methylnoradrenaline was more potent than phenylephrine. However, the ratios between the ED50 for phenylephrine and the ED50 for alpha-methylnoradrenaline in the mesenteric, in the femoral, in the splenic and in the renal circulations was 2.19, 1.89, 1.48, and 1.33, respectively, showing that the relative potency of phenylephrine increased in that order. In the internal carotid vascular bed it was not possible to determine any value. Furthermore, in the renal vascular bed, prazosin (100 micrograms/kg) inhibited pressor responses to all agonists more readily than yohimbine (250 micrograms/kg) and yohimbine was more potent than prazosin against all the agonists in the mesenteric and in the femoral vascular beds. Our results show that: there are both postsynaptic alpha 1- and alpha 2-adrenoceptors in the four vascular beds; the contribution of alpha 2-adrenoceptors to pressor responses to sympathomimetic agents is maximal in the mesenteric followed by the femoral, the splenic and the renal vascular bed, whereas the participation of alpha 1-adrenoceptors is maximal in the renal and progressively smaller in the splenic, in the femoral and in the mesenteric vascular bed, where it reaches the lowest value.