Why the study?
Does cold-induced hypertension cause endothelial dysfunction through reduced eNOS expression in Wistar rats?
Does cold-induced hypertension cause endothelial dysfunction through reduced eNOS expression in Wistar rats?
In a nongenetic, nonsurgical rat model, cold-induced hypertension is associated with endothelial dysfunction driven by reduced eNOS expression.
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Endothelial dysfunction accompanies cold-induced hypertension in rats; leaves open translation to human cold-related cardiovascular risk.
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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Zhu et al. (2002) studied this question.
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