›› 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


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