| Reference : Role of G(i)-proteins in norepinephrine-mediated vasoconstriction in rat tail artery ... |
| Scientific journals : Article | |||
| Life sciences : Biochemistry, biophysics & molecular biology | |||
| http://hdl.handle.net/10993/5721 | |||
| Role of G(i)-proteins in norepinephrine-mediated vasoconstriction in rat tail artery smooth muscle | |
| English | |
| Petitcolin, M. A. [> >] | |
| Spitzbarth-Régrigny, E. [> >] | |
Bueb, Jean-Luc  [University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Life Science Research Unit >] | |
| Capdeville-Atkinson, C. [> >] | |
| Tschirhart, Eric [University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Life Science Research Unit >] | |
| 2001 | |
| Biochemical Pharmacology | |
| Elsevier Science | |
| 61 | |
| 9 | |
| 1169-75 | |
| Yes (verified by ORBilu) | |
| 0006-2952 | |
| Oxford | |
| United Kingdom | |
| [en] physiology ; Norepinephrine ; Muscle, Smooth, Vascular ; Male ; Heterotrimeric GTP-Binding Proteins ; GTP-Binding Protein alpha Subunits, Gi-Go ; GTP Phosphohydrolases ; Cell Membrane ; Calcium ; Biological Transport ; Arteries ; Animals ; Pertussis Toxin ; Prazosin ; drug effects ; metabolism ; cytology ; Virulence Factors, Bordetella ; Vasoconstriction ; Tritium ; Tail ; Signal Transduction ; Receptors, Adrenergic, alpha-1 ; Rats, Wistar ; Rats ; Analysis of Variance | |
| [en] We showed, in rat de-endothelialised tail artery, that pertussis toxin (PTX) (1 microg/mL, 2 hr) attenuated norepinephrine (NE)-induced vasoconstriction without modifying intracellular calcium concentration [Ca2+](i) mobilisation. We suggested the existence of two NE-induced intracellular pathways: a first, which would be insensitive to PTX and lead to [Ca2+](i) mobilisation, and a second sensitive to PTX and involved in the [Ca2+](i) sensitivity of NE-induced contraction. The aim of this study was to demonstrate the existence of the second intracellular pathway. PTX-sensitive G(i/o)-proteins in rat tail artery SMC membrane were identified by immunoblot and ADP-ribosylation. [(32)P]ADP-ribosylation of alpha(i/o)-subunits was demonstrated in situ by perfusing rat de-endothelialised tail artery segments with PTX (1 microg/mL, 2 hr), which suggested that G(i/o)-protein inactivation was involved in the reduction by PTX of the [Ca2+](i) sensitivity of NE-induced contraction. Coupling between G(i/o)-proteins and NE receptors was confirmed by the NE-induced increase in G(i/o)-specific GTPase activity (24.1 +/- 1.9 vs 8.8 +/- 0.4 pmol P(i)/mg protein at 5 min; P < 0.05 vs basal). [(3)H]Prazosin-binding data showed the presence of a heterogeneous alpha(1)-AR population in rat tail artery smooth muscle cells. We demonstrated the in vitro coupling between alpha(1A)-AR subtype and alpha(i)-subunits. In conclusion, we identified, in rat de-endothelialised tail artery, a PTX-sensitive G(i/o)-protein-modulated pathway that is coupled to NE receptors via alpha(1A)-AR. We suggest that NE stimulates two alpha(1)-AR-mediated intracellular pathways: a first, which is mediated by a G(q)-protein and leads to [Ca2+](i) mobilisation and contraction, and a second, which is mediated by a G(i)-protein and is involved in the amplification of the [Ca2+](i) sensitivity of NE-induced tension. | |
| http://hdl.handle.net/10993/5721 |
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