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Calcium antagonists and alpha 2-adrenoceptors: possible role of extracellular calcium ions in alpha 2-adrenoceptor-mediated vasoconstriction.

Authors
  • van Zwieten, P A
  • van Meel, J C
  • Timmermans, P B
Type
Published Article
Journal
Journal of Cardiovascular Pharmacology
Publisher
Ovid Technologies (Wolters Kluwer) - Lippincott Williams & Wilkins
Publication Date
Jan 01, 1982
Volume
4 Suppl 3
Identifiers
PMID: 6184552
Source
Medline
License
Unknown

Abstract

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.

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