Queiroz G, Gonçalves J, Carvalho F, Vale P
Department of Pharmacology, Faculty of Pharmacy, University of Porto, Portugal.
Naunyn Schmiedebergs Arch Pharmacol. 1995 Jan;351(1):60-6. doi: 10.1007/BF00169065.
Release of taurine evoked by electrical stimulation (2700 pulses; 5 Hz; 10 mA unless stated otherwise) and its dependence on noradrenaline and ATP was studied in isolated, perifused rat vas deferens. Outflow of noradrenaline was also measured in some experiments. The basal outflow of taurine averaged 3.90 +/- 0.32 nmol/g tissue per min. Electrical stimulation increased the outflow to about 4 times basal values. The electrically-evoked overflow averaged 128.0 +/- 11.7 nmol/g. An increase in current strength to 40 mA increased the evoked overflow by about 50%. At either current strength, the evoked overflow of taurine (and noradrenaline) was abolished by tetrodotoxin. Ca(2+)-deprivation blocked the overflow of taurine elicited by 10 mA and increased the overflow elicited by 40 mA pulses (but abolished noradrenaline overflow under either condition). Neither prazosin nor pretreatment of the rats with reserpine reduced electrically-evoked overflow of taurine (although reserpine pretreatment abolished evoked noradrenaline overflow). Tyramine (100 mumols/l; 9 min) caused an overflow of taurine 36% of that caused by electrical stimulation (but an overflow of noradrenaline 3 times higher than that evoked by electrical stimulation). Exogenous noradrenaline (9 min) caused a concentration-dependent overflow of taurine with a maximal effect at 162 mumol/l, amounting to 33% of the electrically-evoked overflow. alpha,beta-Methylene ATP (19 mumols/l) elicited an overflow of taurine that faded despite continued exposure to the drug and amounted to 62% of the response to electrical stimulation. Thirty minutes after the start of application of alpha,beta-methylene ATP, electrically-evoked overflow of taurine was greatly reduced. Suramin (100 mumols/l) also reduced taurine overflow in response to electrical stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
在离体灌流的大鼠输精管中,研究了电刺激(2700个脉冲;5赫兹;除非另有说明,电流强度为10毫安)诱发的牛磺酸释放及其对去甲肾上腺素和三磷酸腺苷(ATP)的依赖性。在一些实验中还测量了去甲肾上腺素的流出量。牛磺酸的基础流出量平均为每分钟3.90±0.32纳摩尔/克组织。电刺激使流出量增加到基础值的约4倍。电诱发的溢出量平均为128.0±11.7纳摩尔/克。将电流强度增加到40毫安可使诱发的溢出量增加约50%。在任一电流强度下,河豚毒素均可消除诱发的牛磺酸(和去甲肾上腺素)溢出。钙剥夺可阻断10毫安电流诱发的牛磺酸溢出,并增加40毫安脉冲诱发的溢出(但在两种情况下均消除去甲肾上腺素溢出)。哌唑嗪和用利血平预处理大鼠均未降低电诱发的牛磺酸溢出(尽管利血平预处理可消除诱发的去甲肾上腺素溢出)。酪胺(100微摩尔/升;9分钟)引起的牛磺酸溢出量为电刺激引起的36%(但去甲肾上腺素溢出量比电刺激诱发的高3倍)。外源性去甲肾上腺素(9分钟)引起牛磺酸浓度依赖性溢出,在162微摩尔/升时达到最大效应,相当于电诱发溢出量的33%。α,β-亚甲基ATP(19微摩尔/升)诱发的牛磺酸溢出量尽管持续接触该药物仍会逐渐减弱,相当于电刺激反应的62%。应用α,β-亚甲基ATP 30分钟后,电诱发的牛磺酸溢出量大大减少。苏拉明(100微摩尔/升)也可降低电刺激引起的牛磺酸溢出。(摘要截取自250字)