Vascular Smooth Muscle

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Abstract
In strip preparations from the rabbit main pulmonary artery, it was not possible to differentiate convincingly between α1- and α2-adrenoceptors, when selective agonists such as methoxamine, St 587, B-HT 920, and clonidine, as well as selective antagonists such as prazosin and yohimbine were used for receptor characterization. Measurements of the membrane potential of the vascular smooth-muscle cells with intracellular glass micropipettes showed similar depolarizations in response to the α1-selective methoxamine and the α2-selective B-HT 920. These observations suggest the occurrence of a uniform α-adrenoceptor population in the rabbit main pulmonary artery. However, in contrast to α1-agonists, contractile responses to α2-agonists differed considerably in their dependence on external Ca, as revealed in Ca withdrawal experiments, as well as by the use of Ca antagonists. Furthermore, inactivation of the guanine nucleotide-binding inhibitory protein (Ni protein) by pertussis toxin impaired vasoconstriction, in response to α2-agonists, but left that to α1-agonists unaffected. It is suggested that α1- and α2-agonists induce two distinct conformational changes in an otherwise uniform α-adrenoceptor of the rabbit main pulmonary artery. By the mediation of Ni protein, α2-agonists appear to allow influx of Ca into the vascular muscle cells through a type of Ca channel that is unlikely to be controlled by voltage.

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