Telmisartan reduces mortality and left ventricular hypertrophy with sympathoinhibition in rats with hypertension and heart failure

Takuya Kishi, Yoshitaka Hirooka, Kenji Sunagawa

    研究成果: Contribution to journalArticle査読

    18 被引用数 (Scopus)

    抄録

    BackgroundAngiotensin II type 1 receptor (AT1R) blockers have various benefits on hypertension and/or heart failure. We demonstrated that telmisartan (TLM), an AT1R blocker, causes sympathoinhibition by reduction of reactive oxygen species (ROS) in the rostral ventrolateral medulla (RVLM) of stroke-prone spontaneously hypertensive rats (SHRSPs) the aim of this study was to determine whether TLM improves survival in rats with hypertension and heart failure.METHODSAngiotensin II-infused and salt-loaded SHRSPs were divided into TLM-treated, candesartan cilexetil (CAN)-treated, and control groups. We determined the dose of TLM or CAN with similar depressor effects. We examined survival, urinary norepinephrine excretion (uNE) as a parameter of sympathoexcitation, ROS in the RVLM, and left ventricular (LV) end-diastolic pressure (LVEDP). LV hypertrophy (LVH) was assessed by echocardiography and heart/body weight.RESULTS Compared with the control group, TLM improved survival to a greater extent than CAN. At 4 weeks after treatment, ROS in the RVLM and uNE were significantly lower in the TLM-treated group than in the CAN-treated group, despite the similar depressor effects. At 8 weeks after the treatments, LVH and LVEDP were attenuated in the TLM-treated group compared with the CAN-treated group.CONCLUSIONSOur RESULTS suggest that TLM has the potential to reduce mortality, LVH, and LVEDP and that enhanced sympathoinhibition by reduction of ROS in the RVLM might be one of the mechanisms contributing to the beneficial actions of TLM in a model of rats with severe hypertension and heart failure.

    本文言語英語
    ページ(範囲)260-267
    ページ数8
    ジャーナルAmerican Journal of Hypertension
    27
    2
    DOI
    出版ステータス出版済み - 2 2014

    All Science Journal Classification (ASJC) codes

    • 内科学

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