Roles of cardiovascular autonomic regulation and sleep patterns in high blood pressure induced by mild cold exposure in rats

Increased blood pressure (BP) caused by exposure to cold temperatures can partially explain the increased incidence of cardiovascular events in winter. However, the physiological mechanisms involved in cold-induced high BP are not well established. Many studies have focused on physiological responses to severe cold exposure. In this study, we aimed to perform a comprehensive analysis of cardiovascular autonomic function and sleep patterns in rats during exposure to mild cold, a condition relevant to humans in subtropical areas, to clarify the physiological mechanisms underlying mild cold-induced hypertension. BP, electroencephalography, electromyography, electrocardiography, and core body temperature were continuously recorded in normotensive Wistar-Kyoto rats over 24 h. All rats were housed in thermoregulated chambers at ambient temperatures of 23, 18, and 15 °C in a randomized crossover design. These 24-h physiological recordings either with or without sleep scoring showed that compared with the control temperature of 23 °C, the lower ambient temperatures of 18 and 15 °C not only increased BP, vascular sympathetic activity, and heart rate but also decreased overall autonomic activity, parasympathetic activity, and baroreflex sensitivity in rats. In addition, cold exposure reduced the delta power percentage and increased the incidence of interruptions during sleep. Moreover, a correlation analysis revealed that all of these cold-induced autonomic dysregulation and sleep problems were associated with elevation of BP. In conclusion, mild cold exposure elicits autonomic dysregulation and poor sleep quality, causing BP elevation, which may have critical implications for cold-related cardiovascular events.