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A Physiological Systems Approach to Human and Mammalian Thermoregulation

Effects of chronic cold exposure on the endothelin system

Departments of Medicine and Physiology and Functional Genomics, College of Medicine, University of Florida, Gainesville, Florida

Submitted 7 November 2005 ; accepted in final form 22 December 2005

Cold temperatures have adverse effects on the human cardiovascular system. Endothelin (ET)-1 is a potent vasoconstrictor. We hypothesized that cold exposure increases ET-1 production and upregulates ET type A (ET_A) receptors. The aim of this study was to determine the effect of cold exposure on regulation of the ET system. Four groups of rats (6–7 rats/group) were used: three groups were exposed to moderate cold (6.7 ± 2°C) for 1, 3, and 5 wk, respectively, and the remaining group was maintained at room temperature (25°C) and served as control. Cold exposure significantly increased ET-1 levels in the heart, mesenteric arteries, renal cortex, and renal medulla. Cold exposure increased ET_A receptor protein expression in the heart and renal cortex. ET type B (ET_B) receptor expression, however, was decreased significantly in the heart and renal medulla of cold-exposed rats. Cold exposure significantly increased the ratio of ET_A to ET_B receptors in the heart. An additional four groups of rats (3 rats/group) were used to localize changes in ET_A and ET_B receptors at 1, 3, and 5 wk of cold exposure. Immunohistochemical analysis showed an increase in ET_A, but a decrease in ET_B, receptor immunoreactivity in cardiomyocytes of cold-exposed rats. Increased ET_A receptor immunoreactivity was also found in vascular smooth muscle cells of cold-exposed rats. Cold exposure increased ET_A receptor immunoreactivity in tubule epithelial cells in the renal cortex but decreased ET_B receptor immunoreactivity in tubule epithelial cells in the renal medulla. Therefore, cold exposure increased ET-1 production, upregulated ET_A receptors, and downregulated ET_B receptors.

endothelin type A receptors; endothelin type B receptors; cold-induced hypertension; cardiac hypertrophy

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