Open AccessEffects of Aranidipine, a Novel Calcium Channel Blocker, on Mechanical Responses of the Isolated Rat Portal Vein: Comparison with Typical Calcium Channel Blockers and Potassium Channel Openers
Author(s) -
Keiichi Okumura,
Kenji Ichihara,
Mitsuaki Nagasaka
Publication year - 1997
Publication title -
journal of cardiovascular pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/00005344-199702000-00009
Subject(s) - cromakalim , nicorandil , verapamil , channel blocker , nicardipine , nifedipine , nitrendipine , diltiazem , potassium channel , chemistry , potassium channel blocker , tetraethylammonium , calcium channel , contraction (grammar) , calcium channel blocker , pharmacology , t type calcium channel , charybdotoxin , dihydropyridine , voltage dependent calcium channel , medicine , calcium , potassium , agonist , biochemistry , receptor , organic chemistry
We investigated the effects of aranidipine, a dihydropyridine-type Ca2+ channel blocker, on contractile responses to KCl and spontaneous contractions in isolated rat portal veins in comparison with those of the Ca2+ channel blockers, nifedipine, nicardipine, nitrendipine, diltiazem, and verapamil, and of the K+ channel openers, cromakalim and nicorandil. All the Ca2+ channel blockers concentration-dependently inhibited contractions induced by KCl. Interestingly, aranidipine was more potent against the low K+ (20 mM)-induced contraction than the high K+ (80 mM)-induced contraction, whereas the other Ca2+ channel blockers were equally potent against contractions induced by either concentration of KCl. Cromakalim and nicorandil were effective only on the low K(+)-induced contraction. In addition, all the Ca2+ channel blockers and the K+ channel openers tested inhibited the amplitude of spontaneous contractions of isolated rat portal vein. Tetraethylammonium (TEA), a classic K+ channel blocker, significantly attenuated the effect of aranidipine but not of other Ca2+ channel blockers on the spontaneous contractions. The cromakalim-induced inhibition of spontaneous contractions was antagonized by TEA. Thus aranidipine was found to be different from the typical Ca2+ channel blockers and in part similar to the K+ channel openers in inhibiting mechanical responses of isolated rat portal vein, suggesting that activation of K+ channels may in part in part be involved in the aranidipine-induced vasodilation.