Cell-to-cell signa transduction (cross talk) via ATP on prostate

本研究观察了嘌呤能受体激动剂对电场刺激(EPS)引起的大鼠前列腺内源性去甲肾上腺素(NA)释放的影响。用高效液相色谱结合电化学检测技术对NA进行定量。1)有两种嘌呤受体(PI和P？)抑制大鼠前列腺肾上腺素能神经末梢NA释放。2)高频EPS(8 Hz)诱发的NA通过效应细胞上的α受体诱导嘌呤类物质的释放。EPS引起的嘌呤释放量高于NA释放量(总嘌呤：NA=100：1)。3)刺激效应细胞上的α_1受体所产生的嘌呤作用于连接前的嘌呤受体(PI和P_1)，并抑制NA的释放。4)通过连接前的嘌呤受体抑制NA的释放，从而导致前列腺肌张力下降。5)这些结果表明，高频EPS诱发的过量NA可诱导过度收缩的效应细胞释放大量的嘌呤类物质，从而抑制NA的释放，降低收缩张力，肾上腺素能神经在前列腺平滑肌张力的调控中起重要作用。众所周知，在大多数组织中，NA的释放是由反馈抑制通过连接前的a2-肾上腺素受体来调节的。然而，很少有人尝试研究前列腺中通过连接前嘌呤受体调节神经传递的方法。在这项研究中，我们认为效应细胞中的嘌呤存在跨突触的神经调节作用。

In this study, the effects of purinoceptor agonists on the release of endogenous noradrenaline (NA) evoked electrical field stimulation (EPS) prostate gland of the rat were examined. NA was quantified by HPLC coupled with electrochemical detection techniques. 1) There are two kind of purinoceptors (PI and P?) inhibiting NA-release on adrenergic nerve terminals in rat prostate. 2) NA evoked by high-frequency EPS (8 Hz) induces purines-release via a, receptor on effector cells. The amount of purines-release evoked by EPS was higher than that of NA-release (total purines : NA= 100 : 1). 3) Purines evoked by stimulation of a, receptor on effector cells affect prejunctional purinoceptor (PI and P?), and inhibit NA-release. 4) Inhibition of NA-release via prejunctional purinoceptors consequently induces the decreases of the tone in prostate smooth muscle. 5) These results indicate that excess NA evoked by high frequency EPS induced abundant purines-release from effector cells with excess contraction, and consequently inhibit NA- release and decrease the tone of contraction.The adrenergic nerve plays an important role in the control of prostate smooth muscle tone. It is well known that NA-release is regulated by feedback inhibition through prejunctional a2-adrenoceptors in most tissues. However, very few attempts have been made to investigate the regulation of neurotransmission through prejunctional purinoceptors in the prostate. In this investigation, we suggested the existence of transsynaptic neuromodulation by purines derived from effector cells.