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Related Experiment Videos

Endothelial dysfunction in cold-induced hypertensive rats.

Zhiming Zhu1, Shanjun Zhu, Jijun Zhu

  • 1Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing, PR China. zhuzm@cta.cq.cn

American Journal of Hypertension
|February 28, 2002
PubMed
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Cold exposure causes hypertension in rats by impairing endothelial function, indicated by reduced nitric oxide synthase (eNOS) expression and blunted blood pressure responses to acetylcholine. This suggests a key role for endothelial dysfunction in cold-induced hypertension.

Area of Science:

  • Cardiovascular Physiology
  • Endothelial Function Research
  • Hypertension Pathogenesis

Background:

  • Endothelial dysfunction is present in preatherosclerotic states, but its role in hypertension remains debated.
  • Nitric oxide synthase (NOS) and its product, nitric oxide (NO), are critical for regulating vascular tone and blood pressure.

Purpose of the Study:

  • To investigate the pathogenetic role of endothelial dysfunction in cold-induced hypertension.
  • To evaluate endothelial-dependent changes in blood pressure and endothelial nitric oxide synthase (eNOS) expression in a rat model.

Main Methods:

  • Wistar rats were exposed to cold stress for 8 weeks to induce hypertension.
  • Acetylcholine infusion was used to assess endothelial-dependent vasodilation.
  • N(G)-nitro-L-arginine-methyl ester (L-NAME) was administered to inhibit eNOS.

Related Experiment Videos

  • eNOS expression in aortic vessels was quantified.

    • Main Results:

    • Cold stress significantly increased systolic blood pressure in rats.
    • Acetylcholine-induced blood pressure reduction was significantly attenuated in cold-induced hypertensive rats compared to controls.
    • L-NAME administration increased blood pressure in control rats but had no effect in cold-induced hypertensive rats.
    • eNOS expression was significantly reduced in the aortic vessels of cold-induced hypertensive rats.

    Conclusions:

    • Endothelial dysfunction, characterized by reduced eNOS expression, is evident in this non-genetic, non-surgical model of cold-induced hypertension.
    • Reduced eNOS contributes to the hypertensive phenotype observed in rats exposed to cold stress.