@article{oai:fukuyama-u.repo.nii.ac.jp:00008833,
 author = {Nakamura, Tetsuya and Kerakawati, Rie and Morita, Tetsuo},
 issue = {29},
 journal = {福山大学薬学部研究年報, Annual report of the Faculty of Pharmacy & Pharmaceutical Sciences, Fukuyama University},
 month = {Dec},
 note = {Prazosin is an alpha 1 adrenoceptor antagonist, and it is used as an antihypertensive agent. The effects of prazosin on the activity of hepatic triacylglycerole lipase (HTGL) are not fully understood. In this study, we demonstrated that prazosin stimulates the release of HTGL activity from primary cultures of rat hepatocytes in a time- and dose-dependent manner. U-73122, a phopholipase C (PLC) inhibitor, suppresses prazosin's stimulation of the release of HTGL activity. Moreover, prazosin stimulated the increase of PLC activity in the hepatocytes in a time- and dose-dependent manner. In addition, the prazosin-stimulated release of HTGL activity was reduced by Quin2/AM (an intracellular Ca<sup>2+</sup>-chelator), W-7 (a Calmodulin inhibitor), and KN-93 [an inhibitor of Ca<sup>2+</sup>/Calmodulin dependent protein kinase (CaMK)-II]. These results suggest that the prazosin-stimulated release of HTGL activity is partly due to the activation of CaMK-II that is associated with the elevation of PLC activity in the hepatocytes., Prazosin is an alpha 1 adrenoceptor antagonist, and it is used as an antihypertensive agent. The effects of prazosin on the activity of hepatic triacylglycerole lipase (HTGL) are not fully understood. In this study, we demonstrated that prazosin stimulates the release of HTGL activity from primary cultures of rat hepatocytes in a time- and dose-dependent manner. U-73122, a phopholipase C (PLC) inhibitor, suppresses prazosin's stimulation of the release of HTGL activity. Moreover, prazosin stimulated the increase of PLC activity in the hepatocytes in a time- and dose-dependent manner. In addition, the prazosin-stimulated release of HTGL activity was reduced by Quin2/AM (an intracellular Ca<sup>2+</sup>-chelator), W-7 (a Calmodulin inhibitor), and KN-93 [an inhibitor of Ca<sup>2+</sup>/Calmodulin dependent protein kinase (CaMK)-II]. These results suggest that the prazosin-stimulated release of HTGL activity is partly due to the activation of CaMK-II that is associated with the elevation of PLC activity in the hepatocytes.},
 pages = {41--41},
 title = {プラゾシンによる初代培養ラット肝細胞からの肝性リパーゼの分泌促進(発表論文抄録(2010))},
 year = {2011}
}