自发性高血压大鼠心脏与红细胞L-Arg转运的改变

研究自发性高血压大鼠 (spontaneouslyhypertensiverats ,SHR)心脏L 精氨酸 /一氧化氮 (L Arg/NO)系统的改变及其与红细胞L Arg转运的关系。检测 12周龄 (W)、16W、captopril治疗 4周后的 16WSHR (SHR C)及同龄Wistar Kyoto (WKY)大鼠心脏的L Arg转运、tNOS活性、NO 2 NO 3 和cGMP含量以及红细胞L Arg转运的改变。结果显示 ,SHR心室肌组织L Arg高亲和转运成分的最大转运速率 (Vmax)及低亲和转运成分的米氏常数 (Km)均明显低于WKY大鼠 ;但高亲和转运成分的Km 值和低亲和转运成分的Vmax则无明显改变 ;SHR C组的改变基本同 12W组。心肌组织tNOS活性的变化无统计学意义。NO 2 NO 3 及cGMP含量则分别较WKY组降低 2 4 6 %、19 8% (P >0 0 5 ,P <0 0 5 ,12W组 ) ,5 2 5 %、6 0 4% (P <0 0 1,P <0 0 1,16W组 )和 14 8%、2 3 % (P >0 0 5 ,P <0 0 5 ,SHR C组 )。tNOS活性、cGMP含量与LVW/BW呈负相关 ,r=0 45 0 7,P =0 0 5 (NOS) ,r=0 6 898,P <0 0 1(cGMP)。红细胞L Arg转运的改变与心脏一致 ,且其Vmax与心肌组织高亲和转运成分的Vmax呈正相关 ,r=0 5 6 0 6 ,P =0 0 1;与LVW /BW呈负相关 ,r=- 0 6 2 31,P <0 0 1。以上结果表明 ,SHR心室肌组织L Arg/NO系统活动被抑制 ,其抑制程度与心肌肥厚

The changes in the heart and erythrocyte L-arginine transport of spontaneously hypertensive rats

Changes of L arginine/nitric oxide pathway in heart and of L arginine transport in erythrocytes and their relationship were investigated in spontaneously hypertensive rats (SHR). 12 and 16 weeks old SHR, 16 weeks old SHR with captopril treatment for 4 weeks and 16 weeks old Wistar Kyoto (WKY) rats were used. L arginine transport of myocardial ventricular tissue and erythrocytes, total nitric oxide synthase (tNOS) activity, nitrite and nitrate (NO 2 NO 3) and cyclic GMP (cGMP) content in myocardium were measured. The result showed that in myocardial ventricular tissue of SHR L arginine transport decreased significantly with V max of the high affinity transport being decreased by 24 3% ( P <0 05, 12W group), 36 4% ( P <0.01, 16W group) as compared with WKY group. Michaelis constant (K m) of low affinity transport was significantly lower than that of WKY group. NO 2 NO 3 and cGMP content were respectively decreased by 24 6%, 19 8% ( P >0 05, P <0 05, 12W group), 52 5%, 60 4% ( P <0 05, P <0 01, 16W group) and 14 8%, 23% ( P >0 05, P <0 05, SHR C group) as compared with WKY group. But the K m of L arginine high affinity transport and the V max of low affinity transport and tNOS activity were not significantly changed. In erythrocytes, the changes of L arginine transport coincided with the those of myocardial tissue. The V max had significant positive correlation with the V max of high affinity transport in myocardial tissue, r =0 5606, P =0 01and had negative correlation with left ventricular weight to body weight radio, r =0 6231, P <0 01. These results indicate that the activity of L arginine/nitric oxide pathway inhibited in myocardial tissue of SHR. The correlation between the inhibitory degree of L arginine/nitric oxide pathway and the degree of ventricular hypertrophy is negative. The changes of L arginine transport in erythrocytes coincide with those in myocardium.