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  1. Yun-xia Wang,
  2. Shu-hua Zhang,
  3. Yu-zhi Ge,
  4. Zhi-ting Wu,
  5. Jun Luo,
  6. Yu-zhi Ge
  1. Jiangxi Provincial People's Hospital, Jiangxi Cardiovascular Disease Research Institute


    Objectives Cold is an important factor contributing to the high incidence of hypertension. In order to explore the mechanisms of cold-induced hypertension. This study observed whether Large conductance calcium-activated potassium channel (BKCa) on vascular smooth muscle cells (VSMC) played a role in the development of hypertension during chronic exposure to cold.

    Methods Forty-eight rats were divided into cold-treated group and control group randomly, then, one subgroup of the cold-treated and one subgroup of control rats were sacrificed at 2, 4, 6 and 8 weeks.

    Results Systolic blood pressure started to rise after 2 weeks of cold exposure and continued to increase, reaching a maximal level by the 6th week of exposure to cold, and then pressure begin to decrease slowly throughout the remainder of the experiment. The BKCa current and BKCa peak current density in aortic VSMC increased significantly as the time of exposure to cold went until the 6th week exposure to cold. Furthermore, the expression of L-type Cav1.2 channelα1C subunit mRNA in the cold-treated rats were higher than those in the control rats.

    Conclusions Cold stress increased expression of L-type Cav1.2 channelα1C subunit mRNA, indicate that cytoplasmic Ca2+ concentration increased with cold-treated extended at 6 weeks in the beginning, resulting in increasing blood pressure. BKCa channel currents increased in this progress as the negative-feedback regulators of vascular tone. Our results indicated that activation of BKCa channel could reduce blood pressure (7th and 8th week) in hypertensive subjects.

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