Effects of ambient temperature on cardiovascular and metabolic status of hypertensive and normotensive rats

Abstract

Ambient temperature (T_a) significantly impacts the physiological regulation of several homeostatic systems. Several lines of evidence support the hypothesis that mechanisms associated with regulation of energy balance powerfully affect cardiovascular function. When T_a is low, sympathetic nervous system activity increases, providing for increased nonshivering thermogenesis in support of thermoregulation. Cold exposure increases blood pressure and heart rate, however many early reports stated that the hypertensive effect of cold is delayed for days or weeks. This contrasts the more rapid activation of thermogenesis in brown adipose tissue, which is activated within just a few hours. We hypothesized that cold would produce rapid increases in blood pressure (BP) and heart rate (HR) when BP and HR are measured in undisturbed, unrestrained, radio-telemetered rats. The results reveal that BP and HR are increased within the first 2 hours cold exposure.

Energy expenditure and caloric intake are lower in rats and mice at thermoneutral temperatures (T_a ≈ 28–32°C) compared to typical laboratory conditions (T_a ≈ 21–23°C), indicating that T _a impacts energy balance in rodents. Based on our previous findings that metabolism, food intake, BP, and HR are concurrently increased by cold, we tested the hypothesis that the reduced energy expenditure at thermoneutrality would be associated with lowered BP and HR. Since the increased energy expenditure and cardiovascular effects observed during cold are primarily mediated by sympathetic activation, we tested the hypothesis that β1-adrenergic receptors (β₁-AR) mediate reductions of cardiovascular function at thermoneutrality. To test this hypothesis, we administered the β₁-AR antagonist atenolol to reduce cardiac sympathetic activation prior to thermoneutral exposure. Thermoneutrality produced marked reductions in heart rate and blood pressure, responses that were not prevented by β₁ receptor blockade, suggesting a role for increased parasympathetic activity or decreased intrinsic cardiac activity.

Spectral analysis of the variability of heart rate and blood pressure has been used as a tool for measuring autonomic tone. We utilized spectral analysis to determine whether increased parasympathetic activity occurs during thermoneutrality. The results suggest vagal activation as one mechanism for the bradycardia in hypertensive rats and perhaps differential autonomic tone between normotensive and hypertensive rat strains.