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than, Savineau, unpublished results). is released by stimulation of nonadrenergic, noncholinergic nerves in the rat pulmonary artery (13). More recently, it has been observed in the rabbit pulmonary artery that the release of , ADP, AMP, adenosine in response to electrical field stimulation exceeds that of norepinephrine (25). However, can activate various P2 purinoceptors, i.e., P2X, P2Y, P2u purinoceptors that have been identified cloned (6). P2, PBupurinoceptors belong to the G protein-coupled receptor superfamily (18, 32), whereas PzX purinoceptors belong to the family of transmitter-gated ion channels (5, 31). Both P2X P2Y purinoceptors seem to be present in the smooth muscle of human pulmonary artery (17). Moreover, the pulmonary vasoconstrictor response to in vivo depends, at least in part, on the activation of a PzX purinoceptor (16). produces effects via different excitation-coupling mechanisms may play a modulatory role in a variety of pathophysiological processes such as hypoxic pulmonary vasoconstriction (2 1,22), pulmonary hypertension (22>, the cell cycle progression of vascular (20). We thus designed the present experiments to characterize its action on the [Ca2+]i in the rat pulmonary artery. For this purpose, we investigated the effect of other P2 purinoceptor agonists, 2-methylthio- (2-MeS-), cx$-methylene- (a$-Me), UTP, using indo
AJP - Lung Cellular and Molecular Physiology – The American Physiological Society
Published: Sep 1, 1996
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