This report presents results obtained from many years of study of the effects of prolonged adaptation to cold and noradrenaline on the spike activity of central hypothalamic and peripheral skin thermoreceptors. The involvement of the sympathetic nervous system in forming adaptive changes in the regulatory characteristics of temperature homeostasis and the significance of the various components of thermoreceptor activity to the formation of effector responses are discussed. The roles of different groups of thermoreceptors in forming temperature sensations are analyzed.

Experiments on rats with hereditary stress-induced arterial hypertension showed that hypertension shortened the latency and increased the amplitude of constrictive reaction of skin blood vessels to rapid cooling characterized by more rapid and considerable increase in blood norepinephrine content compared to slow cooling. Decreased thermal threshold of metabolic reaction suggests that arterial hypertension is accompanied by changes in both the vascular walls and tissues involved in metabolic reaction to cooling.

The role of TRP ion channels in the physiological processes is far from clear. In this work we studied the effect of the activation of the peripheral TRPM8 ion channel by its agonist menthol on the cardiovascular parameters in normotensive and hypertensive rats when animals were coming out of anesthesia. The role of the TRPM8 ion channel in the regulation of blood pressure was clearly seen in normotensive animals: Activation of this channel by application of 1% menthol (agonist of TRPM8 ion channel) to skin significantly accelerated the increase in blood pressure and recovery of heart rate when animals come out of anesthesia. The mean rate of pressure rise increased 3 times under the menthol. In hypertensive animals there was weaker and short-time increase in the rate of arterial pressure rise under menthol. Lower sensitivity of hypertensives to menthol is consistent with our previous data on the two fold decrease in the expression of Trpm8 gene in these animals. Recent results evidence that the TRPM8 ion channel is involved in the regulation of blood pressure and this depends on the level of the Trpm8 gene expression. A decrease in the expression of the Trpm8 gene in hypertensives can be a compensatory protection.