Gonçalves J, Bültmann R, Driessen B
Pharmakologisches Institut, Albert-Ludwigs-Universität Freiburg, Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1996 Jan;353(2):184-92. doi: 10.1007/BF00168756.
Effects of isoprenaline on contraction, release of noradrenaline and release of ATP elicited by electrical field stimulation (210 pulses, 7 Hz) as well as on contractions elicited by exogenous noradrenaline and ATP were studied in the isolated vas deferens of the guinea pig. Release of noradrenaline was assessed as overflow of total tritium after preincubation with [3H]-noradrenaline. ATP was measured by means of the luciferin-luciferase technique. In [3H]-noradrenaline-pretreated tissues, electrical stimulation elicited an overflow of tritium and ATP and a biphasic contraction. Isoprenaline (1-100 nM) reduced the contraction, mainly phase I, and enhanced the evoked overflow of tritium: evoked overflow of ATP was not changed significantly. No, or almost no, contraction remained in [3H]-noradrenaline-pretreated tissues exposed to both prazosin (0.3 microM) and suramin (300 microM), and the evoked overflow of ATP was reduced by about 82%. Under these conditions, isoprenaline (1-100 nM) again enhanced the evoked overflow of tritium, but it now decreased the evoked overflow of ATP. Propranolol (1 microM), when added on top of prazosin and suramin, prevented the effects of isoprenaline (1-100 nM). In some tissues not pretreated with [3H]-noradrenaline, purinergic and adrenergic components of the neurogenic contraction (again to 210 pulses, 7 Hz) were isolated by exposure to prazosin (0.3 microM) and suramin (300 microM), respectively. Isoprenaline (1-100 nM) decreased the isolated purinergic component but did not change significantly the isolated adrenergic component. Contractions elicited by ATP (1000 microM) were not changed and contractions elicited by noradrenaline (100 microM) were slightly increased by isoprenaline (1-100 nM). Isoprenaline (100 nM) did not change the degradation of ATP (100 microM) by pieces of the vas deferens. It is concluded that, in the guinea-pig vas deferens, activation of prejunctional beta-adrenoceptors modulates the neural release of noradrenaline and ATP in opposite directions: release of noradrenaline is enhanced, whereas release of ATP is decreased.
在豚鼠离体输精管中,研究了异丙肾上腺素对电场刺激(210次脉冲,7Hz)引起的收缩、去甲肾上腺素释放和ATP释放的影响,以及对外源性去甲肾上腺素和ATP引起的收缩的影响。用[3H] - 去甲肾上腺素预孵育后,通过总氚的溢出评估去甲肾上腺素的释放。ATP通过荧光素 - 荧光素酶技术进行测量。在[3H] - 去甲肾上腺素预处理的组织中,电刺激引起氚和ATP的溢出以及双相收缩。异丙肾上腺素(1 - 100nM)减弱收缩,主要是I期,并增强诱发氚的溢出:诱发的ATP溢出没有显著变化。在同时暴露于哌唑嗪(0.3μM)和苏拉明(300μM)的[3H] - 去甲肾上腺素预处理组织中,没有或几乎没有收缩残留,并且诱发的ATP溢出减少了约82%。在这些条件下,异丙肾上腺素(1 - 100nM)再次增强诱发的氚溢出,但现在减少了诱发的ATP溢出。在哌唑嗪和苏拉明之上加入普萘洛尔(1μM)可阻止异丙肾上腺素(1 - 100nM)的作用。在一些未用[3H] - 去甲肾上腺素预处理的组织中,通过分别暴露于哌唑嗪(0.3μM)和苏拉明(300μM)来分离神经源性收缩(同样为210次脉冲,7Hz)的嘌呤能和肾上腺素能成分。异丙肾上腺素(1 - 100nM)降低分离的嘌呤能成分,但对分离的肾上腺素能成分没有显著影响。ATP(1000μM)引起的收缩没有变化,而去甲肾上腺素(100μM)引起的收缩被异丙肾上腺素(1 - 100nM)轻微增加。异丙肾上腺素(100nM)没有改变输精管碎片对ATP(100μM)的降解。结论是,在豚鼠输精管中,突触前β - 肾上腺素能受体的激活以相反方向调节去甲肾上腺素和ATP的神经释放:去甲肾上腺素的释放增强,而ATP的释放减少。