Abstract

In early studies on the role of calcium in the action of vasoconstrictors, Godfraind and Colleagues (Godfraind et al. 1968; Godfraind and Polster 1968; Godfraind and Kaba 1969) have reported that two pools of calcium are utilized by agonists, one being extracellular, the other intracellular. They also showed that potassium depolarization of vascular smooth muscle required the presence of calcium in the perfusion fluid to produce a contraction. The contraction evoked by calcium in depolarized smooth muscle is dose dependent and is specifically blocked by organic drugs such as cinnarizine, the first agent identified as an organic calcium antagonist (Godfraind and Polster 1968). From their experimental observations, Godfraind and Kaba (1969) have concluded that the inhibition by cinnarizine of the vasoconstriction evoked by catecholamines was due to blockade of calcium entry evoked by the alpha adrenergic agonist. The contraction resistant to cinnarizine blockade was similar to the one recorded in calcium free solution. This latter contraction was insensitive to cinnarizine. The concept of blockade of calcium entry as a main pharmacological action has been extended to several drugs of various chemical structures (see Cauvin et al. 1983; Fleckenstein 1983).KeywordsCalcium AntagonistContractile ResponsePhysiological SolutionCalcium EntryHuman Coronary ArteryThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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