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Hydrochlorothiazide modulates ischemic heart failure-induced cardiac remodeling via inhibiting angiotensin II type 1

Jinghong Luo1,2, Xuanlan Chen1, Chufan Luo1

  • 1Department of Cardiology, First Affiliated Hospital, Zhong-Shan University, Guangzhou, China.

Cardiovascular Therapeutics
|January 1, 2017
PubMed

Insights

Hydrochlorothiazide and valsartan improved cardiac function and reduced fibrosis in rats with heart failure, unlike furosemide. These benefits may stem from inhibiting the angiotensin II signaling pathway.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Renal Physiology

Background:

  • Previous research indicated hydrochlorothiazide's positive effects on cardiac function and fibrosis via the TGF-β/Smad pathway.
  • The role of other diuretics and the angiotensin II receptor type 1 (AT1) signaling pathway in heart failure require further investigation.

Purpose of the Study:

  • To determine if the beneficial effects of hydrochlorothiazide on cardiac function and remodeling are common among diuretics.
  • To investigate the involvement of the angiotensin II receptor type 1 (AT1) signaling pathway in these effects.

Main Methods:

  • Ischemic heart failure was induced in Sprague Dawley rats.
  • Rats were treated with valsartan, hydrochlorothiazide, or furosemide for eight weeks.
  • Neonatal rat ventricular fibroblasts were treated with angiotensin II to assess cellular responses.

Main Results:

  • Hydrochlorothiazide and valsartan significantly improved cardiac function and reduced cardiac interstitial fibrosis compared to controls.
  • Furosemide did not show these beneficial effects.
  • Hydrochlorothiazide reduced AT1, TGF-β, and Smad2 expression, as well as plasma angiotensin II and aldosterone levels, and inhibited angiotensin II-induced TGF-β1 and Smad2 expression in fibroblasts.

Conclusions:

  • The positive effects on cardiac function and remodeling are not universal among diuretics.
  • Hydrochlorothiazide may exert its beneficial effects by reducing left ventricular wall stress and inhibiting the angiotensin II signaling pathway.
Abstract

Keywords:
Cardiac remodelingCongestive heart failureHydrochlorothiazideRenin-Angiotensin-Aldosterone systemTGF-β

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