The effects of nifedipine (1 microM), CdCl2 (0.1 mM) and the Bay K 8644 enantiomers (1 microM) on [3H]noradrenaline release and 45Ca uptake in epididymal and prostatic rat vas deferens were investigated. 2. Nifedipine, CdCl2 and Bay K 8644 optical isomers did not affect the basal tritium release. However, the [3H]noradrenaline release evoked by high potassium (50 mM) from both portions of rat vas deferens was markedly inhibited by CdCl2, scarcely affected by nifedipine and not modified by Bay K 8644 enantiomers. 3. (-)-Bay K 8644 increased the basal and potassium (50 mM) induced 45Ca uptake whereas (+)-Bay K 8644, nifedipine and CdCl2 did not alter the basal 45Ca uptake. However, they strongly inhibited the uptake induced by potassium in both portions of rat vas deferens. 4. These results suggest that the calcium channels (mainly L type) are involved on the contractions in rat vas deferens epididymal and prostatic halves; these channels differ from those present in sympathetic nerve terminals (likely of N Type) which modulates the NA release. 5. This study also shows that Bay K 8644 optical isomers possess opposite effects on the L channels of bisected rat vas deferens smooth muscle.
摘要
研究了硝苯地平（1微摩尔）、氯化镉（0.1毫摩尔）和Bay K 8644对映体（1微摩尔）对大鼠附睾和前列腺输精管中[3H]去甲肾上腺素释放及45钙摄取的影响。2. 硝苯地平、氯化镉和Bay K 8644光学异构体不影响基础氚释放。然而，高钾（50毫摩尔）诱发的大鼠输精管两部分的[3H]去甲肾上腺素释放受到氯化镉的显著抑制，几乎不受硝苯地平影响，且未被Bay K 8644对映体改变。3. （-）-Bay K 8644增加基础和钾（50毫摩尔）诱导的45钙摄取，而（+）-Bay K 8644、硝苯地平和氯化镉不改变基础45钙摄取。然而，它们强烈抑制大鼠输精管两部分中钾诱导的摄取。4. 这些结果表明，钙通道（主要是L型）参与大鼠输精管附睾和前列腺部分的收缩；这些通道不同于交感神经末梢中存在的通道（可能是N型），后者调节去甲肾上腺素释放。5. 本研究还表明，Bay K 8644光学异构体对大鼠输精管平滑肌二分体的L通道具有相反作用。
