Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: Biphasic effect of extracellular ATP on human and rat airways is due to multiple P2 purinoceptor activation. | Respiratory Research BioMed Central Research Open Access Biphasic effect of extracellular ATP on human and rat airways is due to multiple P2 purinoceptor activation Boutchi Mounkaila Roger Marthan and Etienne Roux Address Laboratoire de Physiologie Cellulaire Respiratoire Université Bordeaux 2 Bordeaux F-33076 France Inserm E356 Bordeaux F-33076 France Email Boutchi Mounkaila - m_boutchi@ Roger Marthan - Etienne Roux - Corresponding author Published 08 December 2005 Received 07 October 2005 Accepted 08 December 2005 Respiratory Research 2005 6 143 doi 1465-9921-6-143 This article is available from http content 6 1 143 2005 Mounkaĩla et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Extracellular ATP may modulate airway responsiveness. Studies on ATP-induced contraction and Ca2 i signalling in airway smooth muscle are rather controversial and discrepancies exist regarding both ATP effects and signalling pathways. We compared the effect of extracellular ATP on rat trachea and extrapulmonary bronchi EPB and both human and rat intrapulmonary bronchi IPB and investigated the implicated signalling pathways. Methods Isometric contraction was measured on rat trachea EPB and IPB isolated rings and human IPB isolated rings. Ca2 i was monitored fluorimetrically using indo I in freshly isolated and cultured tracheal myocytes. Statistical comparisons were done with ANOVA or Student s t tests for quantitative variables and X2 tests for qualitative variables. Results were considered significant at P . Results In rat airways extracellular ATP I0-6-I0-3 M induced an epithelium-independent and concentration-dependent
