Neural and hormonal control of arterial pressure during cold exposure in unanesthetized week-old rats

Infant rats respond to cold exposure with increased heat production by brown adipose tissue (BAT). BAT thermogenesis increases steadily with increasing cold exposure, but a point occurs at which thermogenesis can increase no further, resulting in cold-induced bradycardia. Previous work has shown that mean arterial pressure (MAP) is maintained even when cardiac rate decreases as much as 50% from baseline values. We examined the neural and hormonal contributions to peripheral resistance during cold exposure after pups were injected subcutaneously with vehicle, an alpha1-adrenoceptor antagonist (prazosin; 0.5 mg/kg), an ANG II receptor antagonist (losartan; 1 mg/kg), a vasopressin receptor antagonist (Manning compound; 0.5 mg/kg), or simultaneous administration of all three antagonists (triple block). Interscapular temperature, oxygen consumption, cardiac rate, and arterial pressure were monitored as air temperature was sequentially decreased from thermoneutral (i.e., 35 degrees C) to 29, 23, and 17 degrees C. Only pups in the triple block condition exhibited significant decreases in MAP with cooling, even though all pups exhibited substantial decreases in cardiac rate. A followup study suggested that blockade of all three systems was more effective than blockade of any two systems. Finally, at 17 degrees C, ultrasonic vocalizations were accompanied by significant increases in MAP, replicating a previous finding and supporting the hypothesis that the vocalization is the acoustic by-product of the abdominal compression reaction, a maneuver that helps to maintain venous return during cardiovascular challenge.