Driessen B, Goncalves J
Pharmakologisches Institut, Albert-Ludwigs-Universitat Freiburg, Germany.
Eur J Pharmacol. 1996 Feb 5;296(3):261-5. doi: 10.1016/0014-2999(95)00799-7.
Effects of atrial natriuretic peptide (ANP) and 8-bromoguanosine 3':5'-cyclic monophosphate (8-BrcGMP) on contraction, overflow of tritium (after [3H]noradrenaline labelling) and overflow of ATP elicited by electrical field stimulation (210 pulses/7 Hz) were studied in guinea-pig vas deferens. ANP (1-100 nM) slightly increased contractions, did not alter the overflow of tritium but decreased the overflow of ATP by up to 50%. 8-BrcGMP (3-300 mu M) markedly reduced contractions and ATP overflow with no effect on tritium overflow. Contractions were suppressed in the presence of prazosin plus suramin, and evoked overflow of ATP declined to 11%. ANP now gradually increased tritium overflow but again decreased the overflow of ATP. 8-BrcGMP did not change tritium overflow, as before, but increased ATP overflow. The results indicate that ANP inhibits neural release of ATP by a mechanism independent of guanylyl cyclase activation with no major effect on noradrenaline release.
在豚鼠输精管中研究了心房利钠肽(ANP)和8-溴鸟苷3':5'-环一磷酸(8-BrcGMP)对电场刺激(210次脉冲/7赫兹)引起的收缩、氚溢出([3H]去甲肾上腺素标记后)和ATP溢出的影响。ANP(1 - 100纳摩尔)使收缩略有增加,不改变氚的溢出,但使ATP溢出减少高达50%。8-BrcGMP(3 - 300微摩尔)显著降低收缩和ATP溢出,对氚溢出无影响。在哌唑嗪加苏拉明存在的情况下收缩受到抑制,诱发的ATP溢出降至11%。此时ANP逐渐增加氚溢出,但再次降低ATP溢出。8-BrcGMP如前一样不改变氚溢出,但增加ATP溢出。结果表明,ANP通过一种独立于鸟苷酸环化酶激活的机制抑制神经源性ATP释放,对去甲肾上腺素释放无主要影响。