Norepinephrine (NE) and epinephrine (Epi) concentrations in arterial plasma and in skin tissue were measured chromatographically before and after external cooling. Urethan-anesthetized rats were cooled either slowly (0.004–0.006°C/s) or rapidly (0.03– 0.05°C/s). Blood samples were drawn three times from each animal: 1) before cooling and at a rectal temperature decreased 2) by 0.5°C and 3) by 3–4°C. Skin samples were taken from controls and from rapidly or slowly cooled rats at a rectal temperature lowered by 0.5°C. The resting mean values were 36.7 ± 0.3°C for rectal temperature, 0.62 ± 0.079 and 1.09 ± 0.203 ng/ml for plasma NE and Epi, and 85.6 ± 4.1 and 137.6 ± 34.3 ng/g for skin NE and Epi. A decrease in rectal temperature by 0.5°C at rapid cooling produced a 2.6-fold increase of NE and a 2.8-fold increase of Epi in plasma. Concomitantly, there was a significant decrease in skin NE concentration by 28% and Epi by 86%. At a rectal temperature decreased by 0.5°C after slow cooling, plasma catecholamines did not change; at unaltered skin NE concentration, there was a reduction in skin Epi concentration (60%). When rectal temperature was lowered by 3–4°C, the increase in plasma NE was virtually the same at both cooling rates and only plasma Epi increased more after deep rapid cooling than slow cooling. Thus the sympathoadrenal system may be differently activated depending on cooling rate. Rapid cooling, when the dynamic activity of the skin cold receptors is involved in the cold response, may provide conditions for an earlier activation of the sympathoadrenal system. This may evidence the functional significance of the dynamic activity of the skin cold receptors in the formation of the cold defense responses.
Objective: The widespread essential hypertension, of which the nature is still unclear, demands a comprehensive study of the differences between normo-and hypertensives. Hypertension may be associated with changes in the central nervous system functioning, at various levels. Our previous data have shown the differences in thermo-responsiveness of normotensive and hypertensive rats. Thermosensitive TRP (transient receptor potential) ion channels which are considered as a molecular basis of the thermosensitivity are essential for thermoregulation. Hypothalamus is the important brain structure for blood pressure and temperature regulation. The aim of present work was to assess the expression of thermosensitive TRP ion channel genes in functionally different parts of hypothalamus in normo-and hypertensive rats. Methods: Male inherited stress-induced arterial hypertensive (ISIAH) rats and normotensive Wistar Albino Glaxo (WAG) were used. Gene expression was assayed by the quantitative method of reverse transcription-polymerase-chain-reaction (RT-PCR). Results: Differences between normal and hypertensive rats were found in the expression of transient receptor potential melastatin 8 (Trpm8) and transient receptor potential vanilloid 4 (Trpv4) genes. The level of Trpm8 mRNA in the anterior hypothalamus of hypertensives was more than twice lower than in normotensives. In hypertensives, the level of Trpv4 mRNA in posterior hypothalamus was half time higher than in anterior, and significantly higher than in the normotensives. In normotensives, the Trpv4 gene expression was the same in both parts of hypothalamus. Some differences between anterior and posterior hypothalamus were similar in normo-and hypertensives: the level of Trpm8 mRNA in the anterior hypothalamus was three times higher than in the posterior and the levels of Trpv1 and transient receptor potential ankyrin 1 (Trpa1) mRNA, vice versa. Conclusion: The obtained data allow to come closer to understand the possible molecular bases of the status of hypertension and elucidate some aspects of the physiological role of the investigated thermosensitive TRP ion channels.
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