PPAR Research / 2014 / Article / Tab 1

Research Article

TRPV1 Activation Attenuates High-Salt Diet-Induced Cardiac Hypertrophy and Fibrosis through PPAR-δ Upregulation

Table 1

Cardiac function from WT and TRPV1−/− mice on ND, HS or HS + Cap diet for 1 year.

ParameterWTTRPV1−/−
NDHSHS + CapNdHSHS + Cap

No.888888
BW, g27.9 ± 4.227.5 ± 3.226.9 ± 3.830.7 ± 2.026.1 ± 2.3 26.2 ± 2.2
LVEDD, 10−5 m233 ± 29287 ± 36**245 ± 35#219 ± 44280 ± 36288 ± 50
LVESD, 10−5 m158 ± 27211 ± 28**168 ± 22## 147 ± 32208 ± 25††218 ± 31††
LVPW, 10−5 m79 ± 16103 ± 16*75 ± 15## 72 ± 1591 ± 1288 ± 9
%FS32 ± 426 ± 2**31 ± 5# 33 ± 6 26 ± 424 ± 6
LVW/BW (mg/g)1.93 ± 0.513.56 ± 0.90**2.08 ± 0.85## 1.58 ± 0.32 2.95 ± 0.632.93 ± 0.67

Data are expressed as the mean ± SEM.
BW, body weight; FS, fractional shortening; LVEDD, LV end-diastolic diameter; LVESD, LV end-systolic diameter; LVPW, LV posterior wall; LVW, LV weight; WT wild-type mice; TRPV1−/− TRPV1-null mice; NS normal-salt diet; HS high-salt diet; HS + Cap high-salt plus capsaicin diet; *   ** versus WT-NS; #   ## versus WT-HS;   †† versus TRPV1−/−-NS.