Effects of UTP on membrane current and potential in rat aortic myocytes.

The electrophysiological effects of UTP on freshly isolated rat aortic myocytes were examined using the perforated patch clamp technique. Application of alpha,beta-methylene ATP (alphabeta-meATP) and UTP, putative P2X and P2Y2 or P2Y4 purinoceptor agonists, induced transient and oscillatory inward currents, respectively. Experiments with Cl- channel blockers and different external Cl- concentrations demonstrated that the oscillatory current elicited by UTP is attributable to activation of Cl- channels. The transient component elicited by (alphabeta-meATP appeared to be responsible for a non-selective cationic current. With internal application of low-molecular-weight heparin, a blocker of inositol 1,4,5-trisphosphate (InsP3), the oscillatory current elicited by UTP was abolished. The oscillatory current was activated in an all-or-none manner by UTP over the concentration range 0.1 and 1 microM and the frequency and amplitude were independent of the UTP concentration. Under current-clamp mode, UTP produced an oscillatory membrane potential. These results show that rat aortic myocytes have at least two types of P2 receptors. Activation of the P2Y receptor by UTP produces InsP3, which releases Ca2+ from the store site. The resulting increase in intracellular Ca2+ concentration causes the oscillatory Cl- current and the subsequent membrane potential changes.