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Nifedipine abolished active tone and the contractile response to phorbol dibutyrate (PDBu; 10 nM) with the same potency (IC<jats:sub>50<\/jats:sub>= 8 nM), whereas 300 nM PDBu responses were only partially blocked by nifedipine. The classical and novel PKC inhibitors GF-109203X (IC<jats:sub>50<\/jats:sub>= 1\u20132 \u03bcM) and chelerythrine (IC<jats:sub>50<\/jats:sub>= 4\u20135 \u03bcM) and the classical PKC inhibitor G\u00f6-6976 (IC<jats:sub>50<\/jats:sub>= 0.3\u20130.4 \u03bcM) blocked both active tone and 10 nM PDBu responses with similar potency. Active tone development was associated with depolarization of membrane potential ( E<jats:sub>m<\/jats:sub>) and a shift to the left of the E<jats:sub>m<\/jats:sub>-vs.-contraction relationship determined by varying extracellular potassium. The depolarization and leftward shift were reversed by either chelerythrine (10 \u03bcM) or SNP (30 nM). PDBu (100\u2013300 nM) increased peak L-type calcium channel (Ca<jats:sub>v<\/jats:sub>) currents in isolated coronary myocytes, and this effect was reversed by chelerythrine (1 \u03bcM) or G\u00f6-6976 (200 nM). SNP (500 nM) reduced Ca<jats:sub>v<\/jats:sub>currents only in the presence of the PKA blocker 8-bromo-2\u2032- O-monobutyryl-cAMPS, Rp isomer (10 \u03bcM). In conclusion, active tone development in coronary artery is suppressed by basal NO release and is dependent on both enhanced Ca<jats:sub>v<\/jats:sub>activity and classical PKC activity. Both E<jats:sub>m<\/jats:sub>-dependent and -independent processes contribute to contraction. 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