title: [The changes in the heart and erythrocyte L-arginine transport of spontaneously hypertensive rats].
abstract: 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.
authors.affiliation: Department of Physiology, Guangdong Medical College, Zhanjiang 524023, China. hzzheng@gdmc.edu.cn
authors.forename: H Z
authors.initials: HZ
authors.lastname: Zheng
authors.forename: X H
authors.initials: XH
authors.lastname: Wang
authors.forename: X Y
authors.initials: XY
authors.lastname: Liu
authors.forename: C S
authors.initials: CS
authors.lastname: Tang
authors.forename: N K
authors.initials: NK
authors.lastname: Liu
mesh_terms: D000818:Animals; D001120:Arginine / Q000378:metabolism*; D001692:Biological Transport; D002216:Captopril / Q000494:pharmacology; D004912:Erythrocytes / Q000378:metabolism*; D006973:Hypertension / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY
chemical_list: D009569:Nitric Oxide; D001120:Arginine; D002216:Captopril; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat