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In rat thoracic aorta, 12-0-tetradecanoyl-phorbol-13-acetate (TPA) caused a slowly onset, sustained vascular contraction. The contraction was markedly reduced in the absence of extracellular Ca2+, although small tension development was still observed. The tension developed by TPA in the presence of Ca2+ was decreased by serial addition of a Ca2+-channel blocker, verapamil in a concentration-dependent manner. TPA could cause vascular contraction to almost maximum level at lower concentration of extracellular Ca2+, compared with KCl- or norepinephrine-induced contraction. These results suggest that extracellular Ca2+ which influxes through Ca2+-channels into cytoplasm is necessary for full tension development by TPA, and that TPA increases sensitivity of contractile mechanisms coupling with Ca2+.
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