Calcium antagonists and alpha 2-adrenoceptors: possible role of extracellular calcium ions in alpha 2-adrenoceptor-mediated vasoconstriction
Van Zwieten, P.A.; van Meel, J.C.; Timmermans, P.B.
Journal of Cardiovascular Pharmacology 4(Suppl 3): S273-S279
1982
ISSN/ISBN: 0160-2446 PMID: 6184552 Document Number: 184418
A survey concerning the influence of calcium antagonists on the vasoconstriction induced by the selective stimulation of either postsynaptic alpha 1- or alpha 2-adrenoceptors in the resistance vessels of pithed rats and cats, as well as in ganglion-blocked rabbits, is presented. In every species studied, all calcium antagonists (organic: verapamil, D 600, diltiazem, nifedipine, nisoldipine, and a variety of new compounds; inorganic: Co2+, Ni2+, and Mn2+) significantly reduced the pressor response towards the stimulation of postsynaptic vascular alpha 2-adrenoceptors with B-HT 920 (and other agonists). However, the various calcium antagonists showed little influence on the vasoconstriction provoked by the excitation of vascular postsynaptic alpha 1-adrenoceptors. A correlation study revealed that there exists a close correlation between the depressant influence of the calcium-antagonistic drugs on the vasoconstriction due to alpha 2-adrenoceptor stimulation and the calcium-antagonistic potency in vitro. Accordingly, it is speculated that the vasoconstriction due to alpha 2-receptor stimulation requires the influx of calcium ions from the extracellular space across the membrane. This process is obviously sensitive to the influence of calcium-antagonistic drugs.