Abstract: FR-PO268

Change in Fibroblast Growth Factor 23 during the Progression of Left Ventricular Hypertrophy in Hypertensive Model Rats

Session Information

Category: Mineral Disease

  • 1202 Mineral Disease: Vitamin D, PTH, FGF-23

Authors

  • Fujii, Hideki, Kobe University Graduate School of Medicine, Kobe, Japan
  • Watanabe, Kentaro, Kobe University Graduate School of Medicine, Kobe, Japan
  • Kono, Keiji, Kobe University Graduate School of Medicine, Kobe, Japan
  • Goto, Shunsuke, Kobe University Graduate School of Medicine, Kobe, Japan
  • Watanabe, Shuhei, Kobe University Graduate School of Medicine, Kobe, Japan
  • Nishi, Shinichi, Kobe University Graduate School of Medicine, Kobe, Japan
Background

Many clinical studies have demonstrated that serum fibroblast growth factor-23 (FGF23) levels are significantly associated with left ventricular hypertrophy (LVH). Although LVH is frequently observed in hypertensive patients, no experimental and clinical data have proved that FGF23 induces LVH in these patients. A previous study showed that subjects with high serum FGF23 levels may lead to hypertension in the future. Thus, the association between FGF23, hypertension, and LVH is very complexed and remains unknown.
The purpose of our study was to examine the change in serum and intracardiac FGF23 during the progression of hypertension using spontaneously hypertensive rats (SHR).

Methods

We used male SHRs (HT group) and Wistar Kyoto rats (WKY) as a control group in the present study. At 10 weeks, urinary and blood biochemical analyses and blood pressure measurements were performed for these rats. At 18 weeks, the rats were sacrificed and urinary and blood biochemical analyses and real time PCR were performed in the two groups.

Results

At baseline, serum calcium, phosphate and FGF23 levels were comparable between the two groups. Although serum creatinine levels were also comparable, blood pressure, urinary excretion of albumin and serum NT-pro BNP levels were significantly elevated in the HT group compared to the control group. At 18 weeks, relative heart weight and serum NT-proBNP levels were significantly greater in the HT group. In addition, serum calcium and phosphate levels were significantly lower and serum FGF23 levels were significantly higher in the HT group than in the control group. Further analysis showed that mRNA expression of FGF23 in the heart was significantly increased in the HT group than in the control group. Both serum FGF23 levels (r=0.63, p<0.05) and intracardiac mRNA expression of FGF23 (r=0.79, p<0.05) were significantly correlated with relative heart weight.

Conclusion

During the progression of hypertension, serum FGF23 levels were elevated and LVH progressed. Although it is not known whether change in FGF23 is a cause or result of LVH, we suggest that FGF23 is associated with the development of LVH in hypertension.