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

Takuya Kishi, Yoshitaka Hirooka, Kenji Sunagawa

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Abstract

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.

Original languageEnglish
Pages (from-to)260-267
Number of pages8
JournalAmerican Journal of Hypertension
Volume27
Issue number2
DOIs
Publication statusPublished - Feb 1 2014

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Left Ventricular Hypertrophy
Heart Failure
Hypertension
Mortality
Reactive Oxygen Species
Blood Pressure
Hypertrophy
Norepinephrine
telmisartan
Control Groups
Inbred SHR Rats
Echocardiography
Salts
Stroke
Body Weight
candesartan cilexetil

All Science Journal Classification (ASJC) codes

  • Internal Medicine

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Telmisartan reduces mortality and left ventricular hypertrophy with sympathoinhibition in rats with hypertension and heart failure. / Kishi, Takuya; Hirooka, Yoshitaka; Sunagawa, Kenji.

In: American Journal of Hypertension, Vol. 27, No. 2, 01.02.2014, p. 260-267.

Research output: Contribution to journalArticle

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N2 - 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.

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