Zheng H Z, Wang X H, Liu X Y, Tang C S, Liu N K
Department of Physiology, Guangdong Medical College, Zhanjiang 524023, China.
Sheng Li Xue Bao. 2000 Aug;52(4):323-8.
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 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=0.01 and 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.
在自发性高血压大鼠（SHR）中，研究了心脏中L-精氨酸/一氧化氮途径的变化以及红细胞中L-精氨酸转运情况及其相互关系。使用了12周龄和16周龄的SHR、接受卡托普利治疗4周的16周龄SHR以及16周龄的Wistar-Kyoto（WKY）大鼠。测量了心肌心室组织和红细胞中L-精氨酸的转运、总一氧化氮合酶（tNOS）活性、心肌中亚硝酸盐和硝酸盐（NO₂ + NO₃）以及环磷酸鸟苷（cGMP）含量。结果显示，与WKY组相比，SHR心肌心室组织中L-精氨酸转运显著降低，高亲和力转运的Vmax降低了24.3%（12周龄组，P<0.05）、36.4%（16周龄组，P<0.01）。低亲和力转运的米氏常数（Km）显著低于WKY组。与WKY组相比，NO₂ + NO₃和cGMP含量分别降低了24.6%、19.8%（12周龄组，P>0.05、P<0.05），52.5%、60.4%（16周龄组，P<0.05、P<0.01）以及14.8%、23%（SHR+C组，P>0.05、P<0.05）。但L-精氨酸高亲和力转运的Km、低亲和力转运的Vmax以及tNOS活性无显著变化。在红细胞中，L-精氨酸转运的变化与心肌组织一致。Vmax与心肌组织中高亲和力转运的Vmax呈显著正相关，r = 0.5606，P = 0.01，与左心室重量与体重比值呈负相关，r = 0.6231，P<0.01。这些结果表明，SHR心肌组织中L-精氨酸/一氧化氮途径的活性受到抑制。L-精氨酸/一氧化氮途径的抑制程度与心室肥厚程度呈负相关。红细胞中L-精氨酸转运的变化与心肌中的变化一致。
