1 The effects of purinoceptor ligands for P2X 1 and/or P2X 3 receptors (a,b-meATP, IP 5 I, TNP-ATP, MRS 2179, PPADS, Phenol red and RO116-6446/008; i.v., n ¼ 4-5) and for P2Y 1 receptors (PPADS, MRS 2179 and MRS 2269; i.v., n ¼ 3-5) were investigated on the distension-evoked 'micturition reflex' in the urethane-anaesthetized female rat. 2 a,b-meATP (180 nmol kg À1 min À1 ), IP 5 I (10, 30 and 100 nmol kg À1 ), TNP-ATP (1 mmol kg À1 ), MRS 2179 (1 mmol kg À1 ) and PPADS (17 mmol kg À1 ) each caused maintained bladder contractions to occur during the infusion of saline into the bladder. PPADS (17 mmol kg À1 min À1 ) had a similar effect when infused intravesicularly. Regular bladder contractions were not observed until the infusion of saline was halted. For IP 5 I, TNP-ATP, MRS 2179 and PPADS, the magnitude of postinfusion isovolumetric contractions was significantly reduced and, for IP 5 I, this action was also associated with a significant reduction in urethral relaxation. Additionally, TNP-ATP caused a significant increase in the pressure and volume thresholds required to initiate a reflex. 3 Phenol red (a P2X 1 /P2X 3 antagonist; 0.1 and 1 mmol kg À1 ) caused a significant increase in the pressure and volume thresholds required to initiate a reflex and, at the higher dose, also caused a reduction in postinfusion isovolumetric contractions. 4 RO116-6446/008 (a P2X 1 -selective antagonist; 1 and 10 mmol kg À1 ) only caused a reduction in postinfusion isovolumetric contractions. 5 It is concluded that P2X 1 and P2X 3 receptors play a fundamental role in the micturition reflex in urethane-anesthetized female rats. P2X 3 receptor blockade raised the pressure and volume thresholds for the reflex, whereas P2X 1 receptor blockade diminished motor activity associated with voiding. P2Y 1 receptors may be involved in inhibition of rat detrusor tone.

1 The e ects of injections i.c.v. of quipazine, (2 mmol kg 71 ) and 1-(2,5-di-methoxy-4-iodophenyl)-2-aminopropane (DOI; 2 mmol kg 71 ) on renal sympathetic and phrenic nerve activity, mean arterial blood pressure (MAP) and heart rate were investigated in a-chloralose anaesthetized rats pretreated with a peripherally acting 5-HT 2 receptor antagonist. 2 Quipazine or DOI caused a rise in MAP which was associated with a tachycardia and renal sympathoinhibition in rats pretreated (i.c.v.) with the antagonist vehicle 10% PEG. These e ects of quipazine were completely blocked by pretreatment with cinanserin (a 5-HT 2 receptor antagonist) and attenuated by spiperone (a 5-HT 2A receptor antagonist). However, pretreatment with SB200646A (a 5-HT 2B/2C receptor antagonist) only blocked the sympathoinhibition, while pretreatment with SB204741 (a 5-HT 2B receptor antagonist) reversed the sympathoinhibition to excitation as it also did for DOI. Quipazine also caused renal sympathoexcitation in the presence (i.v.) of a vasopressin V 1 receptor antagonist. 3 Injection (i.v.) of the V 1 receptor antagonist at the peak pressor response evoked by quipazine alone and in the presence of SB204741 caused an immediate fall in MAP. For quipazine alone the renal sympathoinhibition was slowly reversed to an excitation, while the renal sympathoexcitation observed in the presence of SB204741 was potentiated. In both, the quipazine-evoked tachycardia was una ected.