Vasoconstricting effect in rat aorta caused by thaliporphine isolated from the plant Neolitsea konishii K.

Thaliporphine (0.1-100 microM) produced sustained, concentration-dependent contraction in isolated rings of rat aorta. Thaliporphine (ED50 = 1.5 +/- 0.5 microM) was less potent than endothelin (ED50 = 3.9 +/- 0.4 nM), but was more potent than Bay K 8644 (ED50 = 5.5 +/- 0.6 microM). Thaliporphine also contracted guinea-pig trachea and ileum preparations, and increased the force of beating of rat left atria, but was less potent on these tissues than on rat aorta. Thaliporphine-induced contraction of rat aorta was not affected by prazosin (0.3 microM), atropine (1 microM), saralasin (10 microM) or ketanserin (10 microM). However, the contraction was slightly potentiated by the removal of endothelium. Preincubation of the rat aorta in Ca(2+)-free Krebs solution (containing 1 mM EGTA) for 15 min completely abolished thaliporphine-induced contractions, and the subsequent addition of 3 mM CaCl2 restored thaliporphine-induced contractions to the control level. In rat aorta, thaliporphine-induced contractions were significantly reduced by nifedipine (1-30 nM) or verapamil (0.01-0.3 microM), and significantly increased by Bay K 8644 (0.1 microM) or KCl (20 mM). The pA2 values for nifedipine and verapamil against thaliporphine-induced contractions were 9.4 +/- 0.1 and 8.4 +/- 0.2, respectively. The results indicate that thaliporphine exerts its vasoconstrictor effect on rat aorta mainly by promoting Ca2+ entry.