Effects of Rosiglitazone on Heat Shock Protein and the Endothelin System in Deoxycorticosterone Acetate-Salt Hypertensive Rats.
- Author:
Eun Hui BAE
1
;
In Jin KIM
;
Jeong Woo PARK
;
Seong Kwon MA
;
Ki Chul CHOI
;
Jong Un LEE
;
Soo Wan KIM
Author Information
- Publication Type:Original Article
- Keywords: rosiglitazone; heat-shock proteins; deoxycorticosterone acetate-salt; endothelin-1
- MeSH: Animals; Aorta; Blood Pressure; Creatinine; Desoxycorticosterone; Diet; Dimethylpolysiloxanes; Endothelin-1; Endothelins; Heart; Heat-Shock Proteins; Hot Temperature; Hypertension; Immunoblotting; Kidney; Peroxisomes; Rats; Real-Time Polymerase Chain Reaction; RNA, Messenger; Thiazolidinediones; Up-Regulation
- From:Electrolytes & Blood Pressure 2008;6(1):1-8
- CountryRepublic of Korea
- Language:English
- Abstract: The deoxycorticosterone acetate (DOCA)-salt rat is known as a model of volume dependent hypertension and characterized by increased cardiac endothelin-1 (ET-1) content. Recently, it has been reported that rosiglitazone (RGT), a peroxisome proliferator-activated subtype gamma receptor agonist, shows blood pressure lowering effect. We investigated whether DOCA-salt hypertension is associated with altered expression of heat shock proteins (HSP) and ET-1 in the heart, aorta, and kidney, and whether RGT changes HSP expression and ET-1 in association with its blood pressure lowering effect. Two weeks after the silastic DOCA (200 mg/kg) strips implantation, DOCA-salt rats were randomly divided to receive control diet with or without RGT (10 mg/kg/day) for another 2 weeks. The mRNA expression of ET-1 was determined by real time polymerase chain reaction. The expression of HSP was determined by semiquantitative immunoblotting. In DOCA-salt rats, systolic blood pressure was markedly increased, while creatinine clearance decreased. RGT treatment attenuated high blood pressure and decreased creatinine clearance in DOCA-salt rats. The mRNA expression of ET-1 was increased in DOCA-salt rats compared to controls, which was counteracted by RGT treatment. The protein expression of HSP70, HSP32, and HSP25 was increased in the kidney and heart in DOCA-salt rats, which was attenuated by RGT treatment in the kidney, but not in the heart. In conclusion, increased expression of ET-1 may play a role in the pathogenesis of hypertension in DOCA-salt rats, which was counteracted by the treatment of RGT. Up-regulation of HSP70, HSP32, and HSP25 in the kidney and heart may play a role in organ protection against a variety of stresses.
