Paradoxical augmentation of (-)Bay K 8644-induced calcium influx by nitrendipine.
(-)Bay K 8644 produced a concentration-dependent contraction of porcine coronary artery rings with the maximal contraction at 10(-6) M. Pretreatment of the rings with 10(-6) M nitrendipine inhibited (-)Bay K 8644-induced contraction, while pretreatment with 10(-8) M nitrendipine potentiated the contraction elicited by (-)Bay K 8644. (-)Bay K 8644 (10(-6) M) significantly stimulated Ca2+ influx. Although 10(-8) M nitrendipine never stimulated Ca2+ influx, Ca2+ influx induced by (-)Bay K 8644 was significantly potentiated by pretreatment with 10(-8) M nitrendipine. Pretreatment with 10(-6) M nitrendipine significantly decreased Ca2+ influx in tissues treated with (-)Bay K 8644. Our results suggest that the increased Ca2+ influx might be involved in the mechanisms by which (-)Bay K 8644-induced contraction was potentiated by pretreatment with nitrendipine.
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology*; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D002132:Calcium Radioisotopes; D002417:Cattle; D003331:Coronary Vessels / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D004357:Drug Synergism; D066298:In Vitro Techniques; D007537:Isometric Contraction / Q000187:drug effects; D007700:Kinetics; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D009568:Nitrendipine / Q000494:pharmacology*
D002132:Calcium Radioisotopes; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D009568:Nitrendipine; D002118:Calcium