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Am J Transl Res. 2016 Feb 15;8(2):1295-301. eCollection 2016.

Ranolazine attenuated heightened plasma norepinephrine and B-Type natriuretic peptide-45 in improving cardiac function in rats with chronic ischemic heart failure.

American journal of translational research

Guangqiu Feng, Yu Yang, Juan Chen, Zhiyong Wu, Yin Zheng, Wei Li, Wenxin Dai, Pin Guan, Chunrong Zhong

Affiliations

  1. Department of Gerontology Xiangya Second Hospital of Central South UniversityChangsha 410011, China; Health Care Center, Hainan Provincial People HospitalHaikou 570311, China.
  2. Department of Gerontology Xiangya Second Hospital of Central South University Changsha 410011, China.
  3. Health Care Center, Hainan Provincial People Hospital Haikou 570311, China.

PMID: 27158417 PMCID: PMC4846974

Abstract

As a new anti-anginal agent, ranolazinehas been shown to play a cardioprotective role in regulating myocardial ischemic injury. Given that plasma norepinephrine (NE) and brain natriuretic peptide (BNP, also termed B-type natriuretic peptide-45 in rats) are considered neuron-hormones to indicate heart failure progression. This study aims to examine effects of ranolazine on plasma NE and BNP-45 of rats with chronic ischemic heart failure (CHF). CHF was induced by myocardial infarction following ligation of a left anterior descending artery in adult Sprague-Dawley rats. We hypothesized that ranolazine attenuates the elevated levels of NE and BNP-45 observed in CHF rats thereby leading to improvement of the left ventricular function. Results showed that levels of plasma NE and BNP-45 were increased in CHF rats 6-8 weeks after ligation of the coronary artery. Our data demonstrate for the first time that ranolazine significantly attenuated the augmented NE and BNP-45 induced by CHF (P<0.05 vs. saline control). In addition, a liner relation was observed between NE/BNP-45levels and left ventricular fractional shortening as indication of left ventricular function (r=0.91 and P<0.01 for NE; and r=0.93 and P<0.01 for BNP-45) after administration of ranolazine. In conclusion, CHF increases the expression of NE and BNP-45 in peripheral circulation and these changes are related to the left ventricular function. Ranolazine improves the left ventricular function likely by decreasing heightened NE and BNP-45 induced by CHF. Therefore, our data indicate the role played by ranolazine in improving cardiac function in rats with CHF.

Keywords: Ranolazine; brain natriuretic peptide; myocardial infarction; norepinephrine

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