title: Repetitive hyperthermia attenuates progression of left ventricular hypertrophy and increases telomerase activity in hypertensive rats.
abstract: We investigated the hypothesis that repetitive hyperthermia (RHT) attenuates the progression of cardiac hypertrophy and delays the transition from hypertensive cardiomyopathy to heart failure in Dahl salt-sensitive (DS) hypertensive rats. Six-week-old DS rats were divided into the following five groups: a normal-salt diet (0.4% NaCl) (NS group), a normal-salt diet plus RHT by daily immersion for 10 min in 40°C water (NS+RHT group), a high-salt diet (8% NaCl) (HS group), a high-salt diet (8% NaCl) plus RHT (HS+RHT group), and high-salt diet (8% NaCl) plus RHT with 17-DMAG (HSP90 inhibitor) administration (HS+RHT+17-DMAG group). All rats were killed at 10 wk. Cardiac hypertrophy and fibrosis were noted in the HS group, whereas RHT attenuated salt-induced cardiac hypertrophy, myocardial and perivascular fibrosis, and blood pressure elevation. The phosphorylated endothelial nitric oxide synthase (eNOS) and Akt were decreased in the HS group compared with the NS group, but these changes were not observed in the HS+RHT group. The levels of HSP60, 70, and 90 were elevated by RHT. Moreover, the increased levels of iNOS, nitrotyrosine, Toll-like receptor-4, BNP, PTX3, and TBARS in the HS group were inhibited by RHT. Telomeric DNA length, telomerase activity, and telomere reverse transcriptase (TERT) were reduced in the HS group; however, these changes were partially prevented by hyperthermia. In conclusion, RHT attenuates the development of cardiac hypertrophy and fibrosis and preserves telomerase, TERT activity and the length of telomere DNA in salt-induced hypertensive rats through activation of eNOS and induction of HSPs.
authors.affiliation: Department of Cardiovascular, Respiratory, and Geriatric Medicine, Kyushu University Hospital at Beppu, Japan. joyama@tsurumi.beppu.kyushu-u.ac.jp
authors.forename: Jun-ichi
authors.initials: J
authors.lastname: Oyama
authors.forename: Toyoki
authors.initials: T
authors.lastname: Maeda
authors.forename: Makoto
authors.initials: M
authors.lastname: Sasaki
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Higuchi
authors.forename: Koichi
authors.initials: K
authors.lastname: Node
authors.forename: Naoki
authors.initials: N
authors.lastname: Makino
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D018450:Disease Progression; D005355:Fibrosis; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology; D006979:Hyperthermia, Induced / Q000379:methods*; D017379:Hypertrophy, Left Ventricular / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D051381:Rats; D020303:Rats, Inbred Dahl; D019098:Telomerase / Q000378:metabolism*; D020257:Ventricular Remodeling / Q000502:physiology
chemical_list: D052250:Nitric Oxide Synthase Type III; D019098:Telomerase