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

本研究观察了嘌呤受体激动剂对电场刺激（EPS）大鼠前列腺释放内源性去甲肾上腺素（NA）的影响。NA通过HPLC结合电化学检测技术定量。1)嘌呤受体有两种（PI和P？）抑制大鼠前列腺肾上腺素能神经末梢的NA释放。2)高频EPS（8Hz）诱发的NA通过效应细胞上的α 1受体诱导嘌呤释放。EPS诱发的嘌呤释放量大于NA释放量（总嘌呤：NA= 100：1）。3)刺激效应细胞上的α 1受体诱发的嘌呤影响连接前嘌呤受体（PI和P？），并抑制NA释放。4)因此，通过连接前嘌呤受体抑制NA释放会导致前列腺平滑肌张力降低。5)这些结果表明，高频EPS诱发的过量NA引起效应细胞释放大量嘌呤，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节中起重要作用。众所周知，在大多数组织中，NA的释放通过连接前α 2肾上腺素受体的反馈抑制来调节。然而，很少有人试图通过前列腺中的连接前嘌呤受体来研究神经传递的调节。在这项研究中，我们建议存在的跨突触的神经调节来自效应细胞的嘌呤。

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.