Effects of Moderate Strength Cold Air Activity on Hypertensive Patients

Objective: The mechanism underlying the effects of cold air on hypertensive disorders was investigated in an experimental study examining blood pressure and biochemical indicators. Methods: Zhangye, a city in Gansu Province, China, was selected as the experimental site. Health screening and blood tests were conducted, and 30 cardiovascular disease patients and 30 healthy subjects were recruited. The experiment was performed during a cold event during April 26–April 29, 2013. Blood pressure, norepinephrine (NE), epinephrine(E) and angiotensin II (ANG–II) levels of the 60 subjects were evaluated 24 h before cold air activity (April 26, morning), during cold air activity (at minimum temperature, between 7:00 and 8:00 on April 28), and 24 h after cold air activity (morning of April 29). The change before, during, and after the cold air activity were analyzed. Results: Cold air exposure can cause significant metabolism and secretion of norepinephrine (NE), epinephrine (E) and angiotensin II (ANG-II) in subjects; take the patient group as an example, NE, E, ANG II and systolic blood pressure was 306.86, 78.65, 34.2ng/L and 136.3mmHg, respectively, during the cold air exposure, respectively increased by 148.13, 1.34, 39.1ng/L and 11.6mmHg, compared with that before the cold air exposure. Furthermore, the mean value of NE, E, ANG II and the systolic blood pressure was still maintained at a high level one hour after the end of the cold air exposure, which was 363.39, 81.3, 67.3ng/L and 131.7mmHg respectively, increased by 204.66, 3.99, 26.1ng/L and 7.1mmHg, respectively, compared with before the cold air exposure. The impact of cold air exposure on the change of blood pressure was shown in both cardiovascular patients and healthy people, and the effect on the cardiovascular patients lasted longer. Conclusions: Cold air exposure increases blood pressure in cardiovascular disease patients and healthy subjects via the sympathetic nervous system (SNS) that is activated first and which augments ANG-II levels accelerating the release of the norepinephrine and stimulates the renin-angiotensin system (RAS). The combined effect of these factors leads to a rise in blood pressure. This paper discusses preliminarily the possible mechanism for increasing in human blood pressure leaded by cold air.