Oxodipine, a dihydropyridine-type calcium antagonist, inhibited KCl-induced aortic contraction in rabbits and reduced cardiac force in less potent rat ventricular test-paper contractions. In rat cultured neonatal ventricular myocytes, Oxodipine reduced L-type Ca currents (I) with an IC of 0.24 μM, and against T-type Ca currents (I) with an IC of 0.41 μM. Oxodipine causes constipation in mice and gingival hyperplasia in dogs.

I(CaL):0.24 µM

In aortic rings, Oxodipine (10(-11)-10(-6) M) inhibited in a concentration-dependent manner the contractions induced by high K+ (IC50 = 9.0 +/- 4.0 x 10(-10) M) or by Ca2+ in high K+ solution (IC50 = 6.2 +/- 2.4 x 10(-9) M). In mesenteric resistance vessels, Oxodipine inhibited the contractions induced by high K+(IC50 = 5.2 +/- 3.1 x 10(-10)).[4]

Oxodipine (5, 20, and 50 μg/kg; anesthetized dogs), a new dihydropyridine calcium channel blocker, ineffective at 5 μg/kg, whereas doses of 20 and 50 μg/kg of oxodipine elicited a decrease in blood pressure with no change in heart rate. These results suggest that, in contrast to other first-generation dihydropyridines, oxodipine exerts a relatively specific action on blood vessels without significant intrinsic negative chronotropic properties in anesthetized sinoaortic-denervated dogs.[4]