Mechanism for pressor response to nonexertional heating in the conscious rat

The purpose of this study was to determine the systemic hemodynamic mechanism(s) underlying the pressor response to nonexertional heat stress in the unrestrained conscious rat. After a 60-min control period [ambient temperature (T(a)) 24°C], male Sprague-Dawley rats (260-340 g) were exposed to a T(a) of 42°C until a colonic temperature (T(c)) of 41°C was attained. As T(c) rose from control levels (38.1 ± 0.1°C) to 41°C, mean arterial blood pressure (carotid artery catheter, n = 33) increased from 124 ± 2 to 151 ± 2 mmHg (P < 0.05). During this period, heart rate increased (395 ± 5 to 430 ± 6 beats/min, P < 0.05) and stroke volume remained unchanged. As a result, ascending aorta blood flow velocity (Doppler flow probe, n = 8), used as an index of cardiac output, did not change from control levels during heating, but there was a progressive T(c)-dependent increase in systemic vascular resistance (+30% at end heating, P < 0.05). This systemic vasoconstrictor response was associated with decreases in blood flow (-31 ± 9 and -21 ± 5%) and increases in vascular resistance (94 ± 16 and 53 ± 8%; all P < 0.05) in the superior mesenteric and renal arteries (n = 8 each) and increases in plasma norepinephrine (303 ± 37 to 1,237 ± 262 pg/ml) and epinephrine (148 ± 28 to 708 ± 145 pg/ml) concentrations (n = 12,P < 0.05). These findings indicate that the pressor response to nonexertional heating in the conscious rat is mediated by systemic vasoconstriction. It appears that this systemic vasoconstriction results primarily from sympathetically mediated vasoconstriction in the viscera, which overrides the regional vasodilatory influences of marked increases in circulating levels of epinephrine.