Sympathectomy does not cause supersensitivity to noradrenaline in rat prostate

Abstract

Chemical sympathectomy classically produces a denervation supersensitivity assumed to be due to a general increase in receptor number on smooth muscle. However, we have suggested that denervation results rather in a spread of synaptic alpha1D‐adrenoceptors, resulting in an increased proportion of this subtype. We now examine whether these effects of sympathectomy are dependent on the prior presence of innervated alpha1D‐adrenoceptors by studying rat prostate in which innervated receptors are reported to be alpha1A. Animals were sympathectomised by 6‐hydroxydopamine injection. Contractions to nerve stimulation in prostate were markedly reduced by the alpha1A‐ antagonist RS100329, which was more potent than the alpha1D‐antagonist BMY 7378. Norepinephrine (NE) potency at producing contractions was unchanged by sympathectomy, so that denervation supersensitivity did not occur. RS100329 significantly shifted the potency of NE to a similar extent in tissues from vehicle‐treated and sympathectomised animals. BMY 7378 revealed a small alpha1D‐adrenoceptor component to NE contractions in sympathectomised but not control. Since supersensitivity does not occur in prostate, a tissue without a significant amount of alpha1D‐adrenoceptors, this may imply that the presence of functionally important innervated alpha1D‐adrenoceptors is required for denervation supersensitivity.