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 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. Ca2+-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 mu mol/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 mu mol/l, amounting to 33% of the electrically-evoked overflow alpha,beta-Methylene ATP (19 mu mol/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 mu mol/l) also reduced taurine overflow in response to electrical stimulation. It is concluded that electrical (neural) stimulation releases taurine in rat vas deferens. The release is mainly postjunctional in origin, secondary to ATP release from sympathetic axon terminals, and a consequence of postjunctional P-2X-purinoceptor activation.