Literature DB >> 11560123

Telemetric monitoring of adrenocorticotrophin-induced hypertension in mice.

C G Schyvens1, G J Mangos, Y Zhang, K U McKenzie, J A Whitworth.   

Abstract

1. The mouse is the animal of choice for studies involving genetic manipulation and transgenic and knockout mice are valuable tools for physiological studies. We have studied adrenocorticotrophin (ACTH)- and steroid-induced hypertension in both rat and humans. The aim of the present study was to develop a model of ACTH-induced hypertension in the mouse and to assess a chronically implanted telemetric device for measurement of blood pressure (BP). 2. Male Swiss Outbred and Quackenbush Swiss (QS) mice (35-45 g) were implanted with TA11PA-C20 BP devices (Data Sciences International, St Paul, MN, USA) under isoflurane anaesthesia. Seven to 10 days later, mice were monitored telemetrically for baseline BP for 4 days. Mice were then randomly allocated to: (i) sham treatment with normal saline s.c.; or (ii) ACTH at 500 microg/kg per day, s.c. Mice were monitored 24 h/day for 10 days. 3. Sham treatment (n = 7) did not affect BP (114 +/- 2/84 +/- 1 to 115 +/- 2/84 +/- 1 mmHg; P = NS). Adrenocorticotrophin treatment (n = 5) raised BP from 112 +/- 7/82 +/- 4 to 138 +/- 3/104 +/- 4 mmHg, which was significantly different from sham treatment (P = 0.0021 for systolic BP; P < 0.0001 diastolic BP). The increase in BP with ACTH was comparable with that seen in previous studies in humans, sheep and rat. Sham and ACTH-treated animals each lost 3% bodyweight. 4. Administration of ACTH (500 microg/kg per day) raises BP in two strains of mice, measured using a telemetry system. This model will allow the selective use of transgenic and/or knockout mice to further elucidate the mechanism of ACTH- and steroid-induced hypertension.

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Year:  2001        PMID: 11560123     DOI: 10.1046/j.1440-1681.2001.03516.x

Source DB:  PubMed          Journal:  Clin Exp Pharmacol Physiol        ISSN: 0305-1870            Impact factor:   2.557


  3 in total

1.  Knockout of the Na,K-ATPase α2-isoform in cardiac myocytes delays pressure overload-induced cardiac dysfunction.

Authors:  Tara N Rindler; Valerie M Lasko; Michelle L Nieman; Motoi Okada; John N Lorenz; Jerry B Lingrel
Journal:  Am J Physiol Heart Circ Physiol       Date:  2013-02-22       Impact factor: 4.733

2.  Knockout of the Na,K-ATPase α₂-isoform in the cardiovascular system does not alter basal blood pressure but prevents ACTH-induced hypertension.

Authors:  Tara N Rindler; Iva Dostanic; Valerie M Lasko; Michelle L Nieman; Jonathan C Neumann; John N Lorenz; Jerry B Lingrel
Journal:  Am J Physiol Heart Circ Physiol       Date:  2011-08-19       Impact factor: 4.733

3.  Antihypertensive effects of selective prostaglandin E2 receptor subtype 1 targeting.

Authors:  Youfei Guan; Yahua Zhang; Jing Wu; Zhonghua Qi; Guangrui Yang; Dou Dou; Yuansheng Gao; Lihong Chen; Xiaoyan Zhang; Linda S Davis; Mingfeng Wei; Xuefeng Fan; Monica Carmosino; Chuanming Hao; John D Imig; Richard M Breyer; Matthew D Breyer
Journal:  J Clin Invest       Date:  2007-09       Impact factor: 14.808

  3 in total

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