The control of uterine contractility during pregnancy and labour is not fully understood. It is not clear whether purinergic receptor agonists have a role in controlling contractility of the pregnant uterus. A1 and A2 receptors have been reported in the pregnant and non-pregnant Guinea-pig myometrium (Smith et al., 1988; Schiemann & Buxton, 1991; Haynes & Pennefather, 1993). A and P2 receptors have been reported in the non-pregnant rat uterus (Gillman & Pennefather, 1998). Evidence for a contractile effect of P2 agonists has been reported in pregnant human myometrium (Ziganshin et al., 2002). The aim of the study was to investigate the effects of purinergic agonists and antagonists on isolated pregnant rat uterus. Uterine strips from young adult female Wistar rats at 19 days of gestation were set up in organ baths at 37 °C, bathed in Krebs buffer and gassed with 95% O2/5% CO2. Spontaneous contractions were recorded via a force transducer and a Powerlab computer set up (AD Instruments). Tissues were allowed to equilibrate for 1 hour and were then exposed to a dose of 45 mM KCl to induce a reference full contraction. A dose range of adenosine, ATP, ADP and UTP of 10-9 - 5 x 10-4 M was applied to the tissue (n = 10 for each agonist). Time-matched controls (n = 10) were run simultaneously using Krebs buffer vehicle. Spontaneous contractions were recorded for 10 minutes post dose. Amplitude, frequency, baseline tone and integral of the contractions over ten minute periods were analysed. The integral was expressed as a percentage of the initial integral of the contraction due to KCl. The experiments were repeated in the presence of antagonists: reactive blue 2 (P2 antagonist), MRS 1191 (A3 antagonist) and 8-cyclopentyl-1,3-dipropylxanthine (A1 antagonist) (n = 5), and using a selective P2X agonist: ATP significantly increased the amplitude of spontaneous contractions (P<0.05) and significantly decreased the frequency of contractions (P<0.05), compared to control, and this action was inhibited by reactive blue 2. Gillman T.A. & Pennefather J.N. (1998) Clin. Exp. Pharmacol. Physiol. 25, 592-599 |