›› 2011, Vol. 31 ›› Issue (4): 392-.doi: 10.3969/j.issn.1674-8115.2011.04.002

• Original article (Basic research) • Previous Articles     Next Articles

Effects of different protein kinase C isoforms on vasodilation induced by propofol

WEN Xiang-yu1,2, WANG Li1, CUI Yong-yao3, JIANG Wei1   

  1. 1.Department of Anesthesiology, The Sixth People's Hospital, Shanghai Jiaotong University, Shanghai 200233, China；2.Department Postgraduate, Soochow University, Suzhou 215006, China；3.Department of Pharmacology, Basic Medical College, Shanghai Jiaotong University, Shanghai 200025, China
  • Online:2011-04-28 Published:2011-04-28
  • Supported by:

    National Natural Science Foundation of China, 30972842；Shanghai Municipal Natural Science Foundation, 09ZR1424000

PDF (PC)

1270

Abstract:

Objective To investigate the relationship between propofol-induced vasodilation and different protein kinase C(PKC) isoforms. Methods Vascular rings of SD rats were randomly divided into endothelium-intact group (n=36) and endothelium-denuded group (n=36), and each group was divided into 6 subgroups: ①10 nmol/L Go6976+1×10-6 mol/L norepinephrine (NA)+ propofol group (n=6)；②10 μmol/L Rottlerin+1×10-6 mol/L NA+propofol group （n=6）；③ 2 μmol/L PKCε-Pseudo+1×10-6 mol/L NA+ propofol group （n=6）；④2 μmol/L PKCθ-Pseudo+1×10-6 mol/L NA+ propofol group（n=6）；⑤2 μmol/L PKCζ-Pseudo+1×10-6 mol/L NA+ propofol group （n=6）；⑥1×10-6 mol/L NA+ propofol group(control group, n=6). PKCα inhibitor Go6976, PKCδ inhibitor Rottlerin, PKCζ-Pseudo, PKCθ-Pseudo and PKCε-Pseudo were used to pretreat isolated thoracic aorta rings for 30 min. Then 1×10-6 mol/L NA evoked a steady maximal vasoconstriction, propofol was added in progressively increasing cumulative concentrations at a 15 min interval (1×10-6, 5×10-6, 1×10-5, 5×10-5 and 1×10-4 mol/L), and the changes of vascular tone were observed. Results In endothelium-intact group, compared with endothelium-intact group, Go6976, PKCε-Pseudo and PKCθ-Pseudo inhibited propofol-induced vasodilation （P<0.05). Rottlerin also inhibited propofol-induced vasodilation, and even reversed the effect (1×10-6 to 5×10-5 mol/L propofol)(P<0.05). In endothelium-denuded group, compared with endotheliumdenuded control group, Rottlerin, PKCθ-Pseudo and PKCε-Pseudo enhanced propofol-induced vasodilation (P<0.05), and Go6976 and PKCζ-Pseudo enhanced vasodilation induced by 1×10-5 to 1×10-4 mol/L propofol (P<0.05). Conclusion PKCα, PKCδ, PKCε and PKCθ involve in propofol-induced vasodilation in intact endothelium.

Key words: propofol, thoracic aorta, vasodilatation, protein kinase C