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Endothelial dysfunction in cold-induced hypertensive rats.

Zhiming Zhu·Shanjun Zhu·Jijun Zhu·Markus van der Giet·Martin Tepel
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Abstract

Endothelial dysfunction can be observed in preatherosclerotic conditions. However, its pathogenetic role in hypertension is still controversial. Endothelial-dependent changes of blood pressure (BP) and expression of endothelial nitric oxide synthase (eNOS) were evaluated in cold-induced hypertensive rats. Wistar rats were exposed to cold stress for 8 weeks. Exposure to cold stress significantly increased the systolic BP in rats. The infusion of acetylcholine significantly lowered mean arterial BP in control rats by 48 +/- 2% and by 32 +/- 1% in cold-induced hypertensive rats. The acetylcholine-induced reduction of mean arterial BP was significantly attenuated in cold-induced hypertensive rats (control rats, 45 +/- 2 mm Hg; cold-induced hypertensive rats, 34 +/- 3 mm Hg; P < .05). Administration of N(G)-nitro-L-arginine-methyl ester for 1 week significantly increased BP in control rats, whereas no effect could be observed in cold-induced hypertensive rats. In cold-induced hypertensive rats eNOS in aortic vessels was significantly reduced compared to control rats. In this nongenetic, nonsurgical animal model of cold-induced hypertensive rats an endothelial dysfunction can be observed due to reduced eNOS.

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AcetylcholineAnimalsAortaBlood PressureCold TemperatureEndothelium, VascularEnzyme InhibitorsHeart RateHypertensionIn Vitro TechniquesMaleNG-Nitroarginine Methyl EsterNitric Oxide SynthaseNitric Oxide Synthase Type IIIRatsRats, WistarVasodilator AgentsJournal ArticleResearch Support, Non-U.S. Gov't

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Zhiming Zhu, Shanjun Zhu, Jijun Zhu, Markus van der Giet, Martin Tepel. 2002. Endothelial dysfunction in cold-induced hypertensive rats.. https://doi.org/10.1016/s0895-7061(01)02268-3

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