Literature DB >> 7197945

Tiapamil, a new calcium antagonist. 1. Demonstration of calcium antagonistic activity and related studies.

R Eigenmann, L Blaber, K Nakamura, S Thorens, G Haeusler.   

Abstract

N-(3,4-Dimethoxyphenethyl)-2-(3,4-dimethoxyphenyl)-N-methyl-m-dithiane-2-propylamine-1,1,3,3-tetraoxide hydrochloride (tiapamil, Ro 11-1781), a new homoveratrylamine derivative, was studied under various experimental conditions which allow the recognition of calcium antagonistic activity, and compared with the reference calcium antagonist verapamil. Similar to verapamil, tiapamil inhibited in a concentration-dependent manner calcium-induced contractions in isolated, potassium-depolarized preparations of rat renal artery, dog coronary artery and rabbit main pulmonary artery. The inhibitory effects of tiapamil and verapamil were overcome by raising the calcium concentration of the bath fluid and a competitive antagonism between calcium ions and both compounds was found. In the rabbit main pulmonary artery both tiapamil and verapamil reduced 45Ca influx into the potassium-depolarized vascular smooth muscle cells. Calcium-mediated slowly rising potentials were evoked in partially depolarized guinea-pig papillary muscles by electrical stimulation in the presence of isoprenaline. Tiapamil, like verapamil, inhibited the slow potentials, an effect which was antagonized by elevation of the concentration of calcium or isoprenaline in the bath fluid. Both tiapamil and verapamil decreased contractile force in isolated guinea-pig atria and papillary muscles as well as in isolated cat hearts. In the last preparation the two compounds also reduced heart rate and increased coronary flow. These results characterize tiapamil as a calcium antagonist in both vascular smooth muscle and cardiac muscle. A comparison between tiapamil and verapamil indicated that both drugs are of approximately equal calcium antagonistic potency in coronary vascular smooth muscle, but verapamil is 5--10 times more potent in smooth muscle of other arterial beds and in cardiac muscle. Thus tiapamil appears to be a calcium antagonist with some preference for coronary vascular smooth muscle.

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Year:  1981        PMID: 7197945

Source DB:  PubMed          Journal:  Arzneimittelforschung        ISSN: 0004-4172


  6 in total

1.  Effect of calcium entry blockers on blood pressure and vasoconstrictor responses to alpha-1 adrenoceptor stimulation in conscious spontaneously hypertensive rats.

Authors:  M J Thoolen; C R Miller; A T Chiu; P B Timmermans
Journal:  Cardiovasc Drugs Ther       Date:  1987-12       Impact factor: 3.727

2.  Excretion of tiapamil in breast milk.

Authors:  D Hartmann; N O Lunell; G Friedrich; A Rane
Journal:  Br J Clin Pharmacol       Date:  1988-08       Impact factor: 4.335

3.  Effects of dauricine on the dose-response relationship of isoproterenol and calcium and on the electro-mechanical activity in cat papillary muscles.

Authors:  G R Li; D C Fang; C J Hu; F H Lü
Journal:  Acta Acad Med Wuhan       Date:  1984

4.  A unitary mechanism of calcium antagonist drug action.

Authors:  K M Murphy; R J Gould; B L Largent; S H Snyder
Journal:  Proc Natl Acad Sci U S A       Date:  1983-02       Impact factor: 11.205

5.  Comparative pharmacokinetics and cardiovascular effects of tiapamil in healthy volunteers and patients with hepatic cirrhosis.

Authors:  P H Hinderling; M Eckert; S Gasic; H G Eichler; R Pötzi; P Heizmann
Journal:  Eur J Clin Pharmacol       Date:  1986       Impact factor: 2.953

6.  Calcium entry blockers inhibit vasoconstrictor responses to sympathetic nerve stimulation mediated by alpha 1-adrenoceptors.

Authors:  M Holck; M Gerold
Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  1985-07       Impact factor: 3.000

  6 in total

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