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Spinal α-adrenoreceptors involved in cardiovascular control have been investigated using selective α-adrenoreceptor agonists and antagonists in urethane-anaesthetized rats., Intrathecal injections of clonidine, α-methylnoradrenaline, guanfacine and M7 at the C7-T1 level reduced blood pressure and heart rate. In contrast, phenylephrine, 5-hydroxytryptamine and procaine had little or no effect. These results suggest the involvement of spinal α2-adrenoreceptors., The fall in blood pressure produced by clonidine appeared to be attributable to a reduction in heart rate and stroke volume. Lower body vascular resistance was unchanged., The clonidine-induced bradycardia was antagonised by prazosin, WB4101, piperoxan or yohimbine. Their relative potencies suggest that α1- rather then α2-adrenoreceptors mediate this response., Piperoxan and yohimbine clearly prevented the clonidine-induced fall in blood pressure; prazosin and WB4101 also appeared to antagonise clonidine but these results were complicated by the fact that these antagonists themselves reduced blood pressure., It was difficult to interpret these results simply in terms of α1- or α2-adrenoreceptors. Thus spinal α-adrenoreceptors may be different from peripheral α1- or α2-adrenoreceptors. [ABSTRACT FROM AUTHOR]

1 Spinal alpha-adrenoreceptors involved in cardiovascular control have been investigated using selective alpha-adrenoreceptor agonists and antagonists in urethane-anaesthetized rats. 2 Intrathecal injections of clonidine, alpha-methylnoradrenaline, guanfacine and M7 at the C7-T1 level reduced blood pressure and heart rate. In contrast, phenylephrine, 5-hydroxytryptamine and procaine had little or no effect. These results suggest the involvement of spinal alpha 2-adrenoreceptors. 3 The fall in blood pressure produced by clonidine appeared to be attributable to a reduction in heart rate and stroke volume. Lower body vascular resistance was unchanged. 4 The clonidine-induced bradycardia was antagonised by prazosin, WB4101, piperoxan or yohimbine. Their relative potencies suggest that alpha 1-rather then alpha 2-adrenoreceptors mediate this response. 5 piperoxan and yohimbine clearly prevented the clonidine-induced fall in blood pressure; prazosin and WB4101 also appeared to antagonise clonidine but these results were complicated by the fact that these antagonists themselves reduced blood pressure. 6 It was difficult to interpret these results simply in terms of alpha 1- or alpha 2-adrenoreceptors. Thus spinal alpha-adrenoreceptors may be different from peripheral alpha 1- or alpha 2-adrenoreceptors.

1. The affinities and efficacies (relative to isoprenaline) of prenalterol and corwin at beta 1- and beta 2-adrenoreceptors, have been determined in isolated cardiac and vascular tissues respectively. 2. Prenalterol and corwin have similar affinities for cardiac beta 1-adrenoreceptors. The affinity of prenalterol for beta 2-adrenoreceptors is approximately 10 times lower than for beta 1-adrenoreceptors; that for corwin is approximately 100 times lower than for beta 1-adrenoreceptors. 3. The efficacies of prenalterol and corwin, relative to isoprenaline, at beta 1 and beta 2-adrenoreceptors, are similar. 4. The greater selectivity of corwin compared with prenalterol, as an agonist at beta 1-adrenoreceptors, is a reflection of its lower affinity for beta 2-adrenoreceptors.

1 We have investigated the influence of chemical sympathectomy or bilateral adrenal demedullation on vasopressor responses produced by the alpha 1-adrenoreceptor agonist, phenylephrine, and the alpha 2-adrenoreceptor agonist, M-7, in pithed rats to see whether either procedure induced selective supersensitivity to either of these compounds. 5-HT, a tryptaminergic vasopressor agent, was also used to discriminate between nonspecific change in vascular responsiveness and those mediated via alpha-adrenoreceptors. 2 Adrenal demedullation caused a slight reduction in the sensitivity to all agonists. Chemical sympathectomy significantly reduced the vasopressor responses to all doses of phenylephrine, but responses to 5-HT were unchanged. In contrast there was a tendency for responses to M-7 to be greater in sympathectomized rats than in untreated rats. 3 It is concluded that circulating adrenal medullary catecholamines do not physiologically modulate vascular alpha-adrenoreceptor function. The differential effect of chemical sympathectomy on the vasopressor responses to phenylephrine and M-7 might be explained in terms of a small increase in the ratio of vascular alpha 2 : alpha 1-adrenoreceptors, that receive a noradrenergic innervation.