scholarly journals Vascular Lesions and Serum Lipid Peroxides in Spontaneously Hypertensive Rats

1978 ◽  
Vol 19 (4) ◽  
pp. 673-673
Author(s):  
Noboru SAITO ◽  
Sakae MUKAINO ◽  
Koichi OGINO
1973 ◽  
Vol 45 (s1) ◽  
pp. 11s-14s
Author(s):  
Kozo Okamoto ◽  
Yukio Yamori ◽  
Shoichiro Nosaka ◽  
Akira Ooshima ◽  
Fumitada Hazama

1. The pathogenesis and complications occurring in spontaneously hypertensive rats (SHR) have been studied. 2. Genetic factors are important both in the development of hypertension and in determining susceptibility to vascular lesions. 3. Selective substrains of SHR may be particularly prone to develop cerebrovascular lesions.


Hypertension ◽  
1980 ◽  
Vol 2 (4) ◽  
pp. 477-489 ◽  
Author(s):  
C Limas ◽  
B Westrum ◽  
C J Limas ◽  
J N Cohn

1978 ◽  
Vol 19 (4) ◽  
pp. 659-659
Author(s):  
Issei NISHIMORI ◽  
Naotaka MIYAGAWA ◽  
Junichi MIYAZAKI ◽  
Toshihiro TAKAGI

Molecules ◽  
2020 ◽  
Vol 25 (14) ◽  
pp. 3269
Author(s):  
Dae Young Lee ◽  
Bo-Ram Choi ◽  
Dahye Yoon ◽  
Hyoung-Geun Kim ◽  
Min-Ho Lee ◽  
...  

Recently, lipidomics has revealed that many diseases are highly associated with altered lipid metabolism, as in the case of hypertension affecting serum lipid metabolism. In this study, an LC–MS-based lipidomic approach was used to profile serum lipids in spontaneously hypertensive rats (SHRs) treated with an extract of Acanthopanax sessiliflorus fruits (ASF), to elucidate the serum lipid metabolism alteration by hypertension and the treatment of a drug or ASF. First, UPLC-QTOF/MS profiled a total of 208 lipids from six pooled samples of normal controls, SHR, SHR + 100 mg/kg of drug, and SHR + ASF 200, 400, or 600 mg/kg. These six groups were differentiated by the PCA and sPLS–DA, and 120 lipid species were identified as differentially regulated lipids (DRLs) by ANOVA (p values < 0.05). Second, UPLC–QqQ/MS was used for the target profiling of 120 DRLs from individual samples of the six groups. Using an ANOVA, 67 lipids (38 TGs, 4 DGs, 17 PCs, 2 PEs, and 6 LPCs) were selected as validated DRLs. The mostly altered lipids, such as TG (62:13), TG (60:13), PC (34:4), PC (36:5), and PC (38:2), were decreased in SHR compared to the normal control, and received little by treatment with ASF. These results demonstrated the correlation between hypertension and serum lipid metabolism. Furthermore, both drug and ASF treatment similarly altered the lipid profiles of SHRs. Finally, we found that DRLs have the potential to help us to interpret the lipid metabolism of hypertension.


1975 ◽  
Vol 39 (1) ◽  
pp. 7-22 ◽  
Author(s):  
FUMITADA HAZAMA ◽  
AKIRA OOSHIMA ◽  
TOSHINARI TANAKA ◽  
KAZUHIKO TOMIMOTO ◽  
KOZO OKAMOTO

2001 ◽  
Vol 2 (1_suppl) ◽  
pp. S84-S90 ◽  
Author(s):  
Daniel Casellas ◽  
Abderraouf Herizi ◽  
Annie Artuso ◽  
Albert Mimran ◽  
Bernard Jover

Our goal was to assess the cardiovascular and renal protection afforded by angiotensin II type 1-receptor blockade against NG-nitro-L-arginine methyl ester (L-NAME)-exacerbated hypertension in young spontaneously hypertensive rats (SHR), in comparison with the antihypertensive drug, hydralazine. Male SHR were assigned to four groups (n=8 per group): no treatment (controls); L-NAME-treated group (20 mg/kg/day, 10 days, orally); co-treatment with L-NAME and hydralazine (15 mg/kg/day, by gavage); co-treatment with L-NAME and candesartan cilexetil (10 mg/kg/day, by gavage), i.e. at a dose that inhibited acute pressor responses to 5—20 ng angiotensin II. One animal died in the L-NAME group, and tail-cuff systolic blood pressure (SBP) increased significantly compared with controls to 201±5 mmHg. Albumin excretion increased 235-fold in L-NAME-treated rats. Heart weight index averaged 3.5±0.1 and 3.8±0.1 mg/g body weight (p<0.05) in control and L-NAME rats, respectively, indicating moderate cardiac hypertrophy induced by L-NAME. Preglomerular vascular lesions affected 63±6% of interlobular arteries and 10±2% of afferent arterioles (vs. 8±3 and 0.8±0.4% in controls, respectively). Hydralazine and candesartan cilexetil treatment similarly reduced SBP to 153±7, and 165±6 mmHg, respectively. However, candesartan provided more protection, in terms of no significant change in albuminuria (vs. 25-fold increase with hydralazine), regression of cardiac hypertrophy, frequency of vascular lesions and histological indices of renal injury maintained within control values. In conclusion, candesartan cilexetil prevented L-NAME-exacerbated hypertension and associated cardio-renal injury in young SHR, the beneficial effects exceeding those of hydralazine.


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