ELECTRICALLY-EVOKED RELEASE OF TAURINE IN THE RAT VAS-DEFERENS - EVIDENCE FOR A PURINOCEPTOR-MEDIATED EFFECT

Release of taurine evoked by electrical stimulation (2700 pulses; 5 Hz ; 10 mA unless stated otherwise) and its dependence on noradrenaline a nd ATP was studied in isolated, perifused rat vas deferens. Outflow of noradrenaline was also measured in some experiments. The basal outflo w of taurine averaged 3.90+/- 0.32 nmol/g tissue per min. Electrical s timulation increased the outflow to about 4 times basal values. The el ectrically-evoked overflow averaged 128.0+/-11.7 nmol/g. An increase i n current strength to 40 mA increased the evoked overflow by about 50% , At either current strength, the evoked overflow of taurine (and nora drenaline) was abolished by tetrodotoxin. Ca2+-deprivation blocked the overflow of taurine elicited by 10 mA and increased the overflow elic ited by 40 mA pulses (but abolished noradrenaline overflow under eithe r condition). Neither prazosin nor pretreatment of the rats with reser pine reduced electrically-evoked overflow of taurine (although reserpi ne pretreatment abolished evoked noradrenaline overflow). Tyramine (10 0 mu mol/l; 9 min) caused an overflow of taurine 36% of that caused by electrical stimulation (but an overflow of noradrenaline 3 times high er than that evoked by electrical stimulation). Exogenous noradrenalin e (9 min) caused a concentration-dependent overflow of taurine with a maximal effect at 162 mu mol/l, amounting to 33% of the electrically-e voked overflow alpha,beta-Methylene ATP (19 mu mol/l) elicited an over flow of taurine that faded despite continued exposure to the drug and amounted to 62% of the response to electrical stimulation. Thirty minu tes after the start of application of alpha,beta-methylene ATP, electr ically-evoked overflow of taurine was greatly reduced. Suramin (100 mu mol/l) also reduced taurine overflow in response to electrical stimul ation. It is concluded that electrical (neural) stimulation releases t aurine in rat vas deferens. The release is mainly postjunctional in or igin, secondary to ATP release from sympathetic axon terminals, and a consequence of postjunctional P-2X-purinoceptor activation.