Thermosensitivity, a possible new locus involved in genetic hypertension.

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Abstract
Spontaneously hypertensive mice have been characterized as more sensitive to environmental heat than normotensive mice. A breeding program was therefore initiated to examine the possible genetic link between thermosensitivity and hypertension. Crossbreeding of spontaneously hypertensive mice with randomly bred normotensive mice produced F1 hybrids, which were then intercrossed to create a F2 population. Thermosensitivity was measured with a noninvasive method. The rate of body temperature increase was significantly (p less than 0.001) higher in the hypertensive mice (1.74 +/- 0.04 degrees C/min) compared with normal controls (1.13 +/- 0.03 degrees C/min). The frequency distribution of the rate of body temperature increase among the progenies was consistent with the hypothesis that a single gene locus determines the observed difference in thermosensitivity between normal and hypertensive mice. The allele that determines the rate of body temperature increase in normal mice was dominant in relation to the allele contributed by hypertensive mice. In the F2 population, a bimodal distribution determined two phenotypes: less than 1.40 degrees C/min and greater than 1.40 degrees C/min. A significant difference (p less than 0.01) in blood pressure of 11 mm Hg was observed between these two phenotypes. In addition, a positive correlation (p less than 0.01) was noted between the rate of body temperature increase and blood pressure in the F2 progeny. We conclude that there is possibly a single locus controlling thermosensitivity, which exhibits additive-dominance inheritance. Alleles of this particular trait segregate in part with an increment in blood pressure. The results support the possibility that the increased thermosensitivity seen in hypertensive mice is associated with one of the genes that contributes to their high blood pressure.