Effect of high blood flow on the expression of endothelial constitutive nitric oxide synthase in rats with femoral arteriovenous shunts

被引:8
作者
Jeon, BH
Chang, SJ
Kim, JW
Hong, YM
Yoon, SY
Choe, IS
机构
[1] Chungnam Natl Univ, Coll Med, Dept Physiol, Taejon 301131, South Korea
[2] Korea Res Inst Biosci & Biotechnol, Mol & Cellular Biol Res Div, Taejon 305600, South Korea
来源
ENDOTHELIUM-JOURNAL OF ENDOTHELIAL CELL RESEARCH | 2000年 / 7卷 / 04期
关键词
nitric oxide; endothelial constitutive nitric oxide synthase; high blood flow; femoral arteriovenous shunt; competitive RT-PCR;
D O I
10.3109/10623320009072211
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The effect of high blood flow on the expression of endothelial nitric oxide synthase has been investigated in the femoral arteriovenous shunt (AVS) rats created by inserting U-shaped polyurethane tubes in the left femoral arteries and veins. Three days after inserting the femoral AVS, the mean aortic blood flow rate in the abdominal aorta of the AVS rats was about 2.0 times higher than that in the control rats (110.0 +/- 8.4 ml/min vs 52.7 +/- 2.7 ml/min, p < 0.001). The competitive reverse transcriptase-polymerase chain reaction (RT-PCR) data revealed that the mRNA expression level of the endothelial constitutive nitric oxide synthase (ecNOS) was increased in the aortas of the femoral AWS rats compared to that in the control rats. Western blot analysis using a monoclonal antibody against ecNOS revealed that the ecNOS protein levels were markedly increased in the aortas of femoral AVS rats, but ecNOS protein levels in aortas without endothelium were not significantly increased. Inducible nitric oxide synthase (iNOS) protein was not expressed in the aortic tissues with and without endothelium in the control rats. This iNOS expression was not increased by the high blood flow in the femoral AVS rats. These findings suggest that high blood flow could up-regulate the expression levels of ecNOS mRNA and proteins in femoral arteriovenous shunt rats.
引用
收藏
页码:243 / 252
页数:10
相关论文
共 26 条
[1]  
ANDO J, 1988, IN VITRO CELL DEV B, V24, P871
[2]   SINGLE-STEP METHOD OF RNA ISOLATION BY ACID GUANIDINIUM THIOCYANATE PHENOL CHLOROFORM EXTRACTION [J].
CHOMCZYNSKI, P ;
SACCHI, N .
ANALYTICAL BIOCHEMISTRY, 1987, 162 (01) :156-159
[3]   FLOW ACTIVATES AN ENDOTHELIAL POTASSIUM CHANNEL TO RELEASE AN ENDOGENOUS NITROVASODILATOR [J].
COOKE, JP ;
ROSSITCH, E ;
ANDON, NA ;
LOSCALZO, J ;
DZAU, VJ .
JOURNAL OF CLINICAL INVESTIGATION, 1991, 88 (05) :1663-1671
[4]   FLOW STIMULATES ENDOTHELIAL-CELLS TO RELEASE A NITROVASODILATOR THAT IS POTENTIATED BY REDUCED THIOL [J].
COOKE, JP ;
STAMLER, J ;
ANDON, N ;
DAVIES, PF ;
MCKINLEY, G ;
LOSCALZO, J .
AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 259 (03) :H804-H812
[5]   CHRONIC ARTERIOVENOUS SHUNT - EVALUATION OF A MODEL FOR HEART-FAILURE IN RAT [J].
FLAIM, SF ;
MINTEER, WJ ;
NELLIS, SH ;
CLARK, DP .
AMERICAN JOURNAL OF PHYSIOLOGY, 1979, 236 (05) :H698-H704
[6]   The 67-kDa laminin-binding protein is involved in shear stress-dependent endothelial nitric-oxide synthase expression [J].
Gloe, T ;
Riedmayr, S ;
Sohn, HY ;
Pohl, U .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (23) :15996-16002
[7]   Flow-induced arterial enlargement is inhibited by suppression of nitric oxide synthase activity in vivo [J].
Guzman, RJ ;
Abe, K ;
Zarins, CK .
SURGERY, 1997, 122 (02) :273-279
[8]   VASOCONSTRICTION AND INCREASED FLOW - 2 PRINCIPAL MECHANISMS OF SHEAR STRESS-DEPENDENT ENDOTHELIAL AUTACOID RELEASE [J].
HECKER, M ;
MULSCH, A ;
BASSENGE, E ;
BUSSE, R .
AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 265 (03) :H828-H833
[9]   PRINCIPLES OF DESIGN OF FLUID TRANSPORT-SYSTEMS IN ZOOLOGY [J].
LABARBERA, M .
SCIENCE, 1990, 249 (4972) :992-1000
[10]   Induction of nitric oxide synthase mRNA by shear stress requires intracellular calcium and G-protein signals and is modulated by PI 3 kinase [J].
Malek, AM ;
Jiang, LW ;
Lee, I ;
Sessa, WC ;
Izumo, S ;
Alpert, SL .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1999, 254 (01) :231-242