ArticleBritish journal of pharmacology1988
Selective modulation by membrane potential of the interaction of some calcium entry blockers with calcium channels in rat mesenteric artery.
Article in British journal of pharmacology, 1988. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 31 citations in OpenAlex.
- Endothelin-1 and endothelin-2 initiate and maintain contractile responses by different mechanisms in rat mesenteric and cerebral arteries.British journal of pharmacology · 2013Article
- Antioxidant effects and the therapeutic mode of action of calcium channel blockers in hypertension and atherosclerosis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2005Review
- Dihydropyridine enantiomers block recombinant L-type Ca2+ channels by two different mechanisms.The Journal of physiology · 1999Article
- Cardioselectivity of calcium antagonists.Cardiovascular drugs and therapy · 1994Review
- Radioligand and functional estimates of the interaction of the 1,4-dihydropyridines, isradipine and lacidipine, with calcium channels in smooth muscle.British journal of pharmacology · 1993Article
- Binding sites for 1,4-dihydropyridine Ca(2+)-channel modulators in rat intestinal smooth muscle.Naunyn-Schmiedeberg's archives of pharmacology · 1991Article
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
1. The effects of flunarizine, (+)-PN 200-110 and nifedipine on [3H]-(+)-PN 200-110 specific binding were investigated in intact rat mesenteric arteries bathed in physiological solution or in KCl-depolarizing solution, and in a membrane fraction from rat mesenteric arteries. 2. Unlabelled dihydropyridines, (+)-PN 200-110 and nifedipine, inhibited [3H]-(+)-PN 200-110 specific binding concentration-dependently in polarized as well as in depolarized intact arteries. The Ki value of (+)-PN 200-110 was decreased in arteries bathed in KCl-depolarizing solution compared to arteries bathed in physiological solution, while the Ki value of nifedipine was not significantly changed. Ki values measured in depolarized arteries were close to the IC50 values (concentrations inhibiting by 50% the KCl-contraction of rat mesenteric artery). 3. Flunarizine (10(-6) M) was unable to displace the specific binding of [3H]-(+)-PN 200-110 in intact arteries bathed in physiological solution. At 10(-7) M-10(-6) M, it inhibited the binding in depolarized arteries, suggesting that prolonged depolarization is required for the interaction of flunarizine with the dihydropyridine receptor. 4. In a membrane fraction isolated from rat mesenteric arteries, (+)-PN 200-110, nifedipine and flunarizine were all able to displace completely the specific binding of [3H]-(+)-PN 200-110. Displacement curves were parallel and Hill coefficients were close to unity. Ki values were close to the values obtained in depolarized intact arteries. 5. These results revealed a good correlation between the data obtained from binding tests and from pharmacological studies for dihydropyridine calcium entry blocking drugs, taking into account the time-dependence associated with their action on KCl-contraction compared to their binding properties. There was an important discrepancy between the concentrations of flunarizine active in binding studies and those active in pharmacological studies, which could be accounted for by the existence of multiple binding sites for calcium entry blockers in calcium channels.
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