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.