Antisympathetic and hemodynamic property of a dual L/N-type Ca(2+) channel blocker cilnidipine in rats

The in vivo antisympathetic property of a dual L/N-type Ca(2+) channel blocker cilnidipine compared with that of typical N-type Ca(2+) channel blockers has never been clarified. We investigated the effects of the drug on a sympathetic nerve-mediated vascular response and vasodilating action in rats...

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Bibliographic Details
Published in:European journal of pharmacology 2002-01, Vol.434 (1-2), p.43
Main Authors: Takahara, Akira, Koganei, Hajime, Takeda, Tomoko, Iwata, Seinosuke
Format: Article
Language:English
Subjects:
Animals
Calcium Channel Blockers - pharmacology
Calcium Channels, L-Type - drug effects
Calcium Channels, N-Type - drug effects
Dihydropyridines - pharmacology
Hemodynamics - drug effects
Male
omega-Conotoxins - pharmacology
Rats
Rats, Sprague-Dawley
Sympatholytics - pharmacology
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Summary:The in vivo antisympathetic property of a dual L/N-type Ca(2+) channel blocker cilnidipine compared with that of typical N-type Ca(2+) channel blockers has never been clarified. We investigated the effects of the drug on a sympathetic nerve-mediated vascular response and vasodilating action in rats in comparison with those of an N-type Ca(2+) channel blocker omega-conotoxin MVIIA. In pithed rats, omega-conotoxin MVIIA preferentially suppressed the sympathetic nerve stimulation-induced pressor response, whereas cilnidipine suppressed the pressor response induced by sympathetic nerve stimulation and angiotensin II. In anesthetized rats, cilnidipine or omega-conotoxin MVIIA decreased mean blood pressure, while heart rate was decreased by omega-conotoxin MVIIA, but slightly increased by cilnidipine. These results suggest that cilnidipine can affect sympathetic N-type Ca(2+) channels in addition to vascular L-type Ca(2+) channels in antihypertensive doses in the rat in vivo. The antisympathetic activity of cilnidipine is not excessive for an antihypertensive drug in comparison with that of omega-conotoxin MVIIA.
ISSN:0014-2999
DOI:10.1016/S0014-2999(01)01521-7