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Year : 2022  |  Volume : 65  |  Issue : 4  |  Page : 179-186

Prazosin improves neurogenic acute heart failure through downregulation of fibroblast growth factor 23 in rat hearts

1 Division of Cardiovascular Surgery, Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
2 Department of Pediatrics, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
3 Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung; Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan
4 Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan

Correspondence Address:
Dr. Hsin-Hung Chen
Department of Medical Education and Research, Kaohsiung Veterans General Hospital, No. 386, Dazhong 1st Rd., Zuoying Dist., Kaohsiung City 813414
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/cjp.cjp_9_22

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Bilateral nucleus tractus solitarii (NTS) lesions, possibly caused by enterovirus 71 infection, cause severe neurogenic hypertension, leading to acute heart failure (HF), pulmonary edema, and death within hours. Alpha-adrenergic blockers attenuate blood pressure and ameliorate HF and pulmonary edema, thereby prolonging survival time. However, the molecular mechanisms of these blockers are not clear. In this study, we investigated these mechanisms in a rat model of 6-hydroxydopamine (6-OHDA)-induced HF. Sprague–Dawley rats were treated with prazosin 10 min after the microinjection of 6-OHDA into the NTS. Immunohistochemistry and dihydroethidium (DHE) staining were used for analysis. In the cardiac tissue of 6-OHDA-induced HF, in situ expression of tumor necrosis factor-alpha (TNF-α), fibroblast growth factor-23 (FGF23), and FGF receptor 1 (FGFR1) increased, but in situ expression of Vitamin D receptor (VDR) decreased. DHE staining revealed several heart cells with high reactive oxygen species production. Prazosin treatment decreased TNF-α, FGF23, and FGFR1 expression in the heart of rats with 6-OHDA-induced HF. It also prevented cardiomyopathy caused by 6-OHDA-induced bilateral NTS lesions by inhibiting the FGF23-FGFR1 pathway and downregulating TNF-α expression. In situ, FGF23, FGFR1, VDR, superoxide, and TNF-α in the heart were found to be involved in acute HF in our rat model of 6-OHDA-induced bilateral NTS lesions. These findings are potentially useful for treating fatal enterovirus 71 infection-induced NTS lesions and HF.

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