Therapeutic Effect of Pitavastatin on Renal Injury Induced by Hypertension
|
Accession number;06A0784853
|
| Title;Therapeutic Effect of Pitavastatin on Renal Injury Induced by Hypertension |
| Author;
HARUNA YOSHISUKE
(Kawasaki Medical School, Dep. Medicine, JPN)
TOMITA NARUYA
(Kawasaki Medical School, Dep. Medicine, JPN)
NAMIKOSHI TAMEHACHI
(Kawasaki Medical School, Dep. Medicine, JPN)
OZEKI MASAHITO
(Kawasaki Medical School, Dep. Medicine, JPN)
KOBAYASHI SHIN'YA
(Kawasaki Medical School, Dep. Medicine, JPN)
KOMAI NORIO
(Kawasaki Medical School, Dep. Medicine, JPN)
SASAKI TAMAKI
(Kawasaki Medical School, Dep. Medicine, JPN)
KASHIHARA NAOKI
(Kawasaki Medical School, Dep. Medicine, JPN)
|
Journal Title;Ther Res
|
Journal Code:Y0681A
|
ISSN:0289-8020
|
|
VOL.27;NO.9;PAGE.1740-1744(2006)
|
| Figure&Table&Reference;FIG.5, TBL.1, REF.12 |
| Pub. Country;Japan |
| Language;Japanese |
| Abstract;Objective: In recent years, attention has been drawn to pleiotropic effects of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor (statin). On the other hand, we reported that hypertensive renal injury is caused by the imbalance of nitric oxide (NO) reactive oxygen species (ROS). We investigated weather pitavastatin has beneficial effects for renal injury induced by hypertension through the increase of NO bioavailability. Method and Results: We used male Dahl salt sensitive rats given a 0.3%NaCl diet (LS), 8%NaCl diet (HS), and 8%NaCl diet plus pitavastatin (2mg/kg) (HS+Pit) for four weeks. Renal ROS and NO production were imaged by confocal laser microscopy after perfusion with dichlorofluorescein diacetate (DCFH-DA) and diaminorhodamine (DAR)-4M AM. In the LS rats, little ROS production and a significant increase in NO production were noticed in glomeruli and vasculature. In contrast, accelerated ROS production and diminished bioavailable NO were observed in the pre-glomerular arteries of HS rats. This imbalance of ROS/NO was ameliorated by pitavastatin. There were no significant changes in plasma parameters and blood pressure between HS and HS+Pit groups. In HS group, urinary protein excretion was significantly increased compared with LS group (p<0.01). This oxidative stress marker was significantly ameliorated in HS+Pit group (p<0.01 vs HS group). In contrast, urinary NOx excretion was significantly increased in HS+Pit group compared to HS group (p<0.01). Moreover, pitavastatin slightly improved histological damages observed in HS group by measuring GS and IF scores. Conclusion: Pitavastatin ameliorates renal injury through the correction of ROS/NO imbalance in Dahl salt sensitive rats. (author abst.) |
|
|
|
Related Articles;
|
|
