Vascular smooth muscle contraction initiated by postsynaptic α2-adrenoceptor activation is induced by an influx of extracellular calcium

Vasoconstriction in pithed, normotensive rats elicited via stimulation of postsynaptic α - 2 -adrenoceptors by B-HT 920 was antagonized by EDTA and the calcium antagonists nifedipine, D 600 and verapamil, whereas pressor responses to the α 1 -agonist methoxamine were unaffected. This indicates that vasoconstriction in vivo initiated via postsynaptic α - 2 -adrenoceptors requires an influx or extracellular calcium. Thus, the antihypertensive affect of calcium antagonists may be based upon a diminution of vascular tone maintained by postsynaptic α - 2 -adrenoceptors.