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

Abstract

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 α1-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°C) to 29, 23, and 17°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°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.