MECHANISMS OF BLADDER EP1THELIUM INDUCE PAIN SENSATION

膀胱的三磷酸腺苷分泌是压力依赖性的(从5cmH2O到45cmH2O)。刺激TRPV1通道、EP1受体(前列腺素E_2受体)或M受体均可增加内质网释放Ca~(2+)的ATP分泌。腺苷环化酶的激活也增加了ATP的分泌，这种作用不依赖于先前的机制。门店操作的钙离子进入抑制了扩张诱导的尿路中ATP的释放。这对于在膀胱中储存尿液期间持续的ATP释放可能是重要的。

ATP secretion from the urinary bladder was observed pressure dependently (from 5cmH_2O to 45cmH_2O). Stimulation of either TRPV1 channel, EP1 receptor (Prostaglandin E_2 receptor) or muscarinic receptor increased ATP secretion which releasing Ca^<2+> from endoplastic reticulum. Activation of adenylate cyclase also increased ATP secretion which independent from previous mechanism. Store-operated Ca^<2+> entry suppressed distention-induced ATP release from urothelim. These could be important for continuous ATP release during the storage of the urine in the urinary bladder.