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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Kanda, Y. Watanabe, Y. |
| Description | Author Affiliation: Kanda Y ( Department of Pharmacology, National Defense Medical College, Tokorozawa, Saitama, Japan. kanda@ndmc.ac.jp) |
| Abstract | BACKGROUND AND PURPOSE: Adrenaline has been implicated in the pathogenesis of atherosclerosis. However, little is known regarding the role of adrenaline in glucose transport in VSMC. EXPERIMENTAL APPROACH: In this study, we examined the effects of adrenaline on glucose uptake in rat VSMC. We also examined the downstream signaling pathway from the beta-adrenoceptor to glucose uptake, using a pharmacological approach. To investigate the downstream action of adenylate cyclase, we studied the effects of GGTI-298, an inhibitor of geranylgeranylation of GTPases, including Rap1. To confirm the involvement of Rap1, we silenced Rap1 by siRNA. KEY RESULTS: Adrenaline induced glucose uptake in a dose-dependent manner. The adrenaline-induced glucose uptake was inhibited by L-propranolol, (a selective beta-adrenoceptor antagonist), but not by prazosin (a selective alpha(1)-adrenoceptor antagonist) or UK14304 (a selective alpha(2)-adrenoceptor antagonist), suggesting the involvement of beta-adrenoceptors in glucose transport. Long-term treatment with cholera toxin, which resulted in sequestration of G(s) proteins, prevented the adrenaline-induced glucose uptake. Forskolin, a direct activator of adenylate cyclase, was found to mimic the effects of adrenaline. Adrenaline-induced glucose uptake was inhibited by GGTI-298, not by H89 (a selective inhibitor of PKA). Silencing of Rap1 by siRNA attenuated the adrenaline-induced glucose uptake. Adrenaline-induced glucose uptake was inhibited by SB203580 (a selective inhibitor of p38MAPK) and adrenaline-induced p38MAPK activation was inhibited by GGTI-298 and siRNA against Rap1. CONCLUSIONS AND IMPLICATIONS: These findings suggest that adrenaline-induced glucose transport is mediated by beta-adrenoceptors, G(s), adenylate cyclase, Rap1, and p38MAPK in vascular smooth muscle cells. |
| ISSN | 00071188 |
| e-ISSN | 14765381 |
| Journal | British Journal of Pharmacology |
| Issue Number | 4 |
| Volume Number | 151 |
| Language | English |
| Publisher | Wiley Online Library(on behalf of The British Pharmacological Society) |
| Publisher Date | 2007-06-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Epinephrine Pharmacology Glucose Metabolism MAP Kinase Signaling System Physiology Muscle, Smooth, Vascular Myocytes, Smooth Muscle P38 Mitogen-Activated Protein Kinases Rap1 GTP-Binding Proteins Animals Biological Transport Drug Effects Cells, Cultured Cyclic AMP-Dependent Protein Kinases Antagonists & Inhibitors GTP-Binding Protein Alpha Subunits, Gs Cytology Rats, Sprague-Dawley Research Support, Non-U.S. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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