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 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.