Abstract
In vivo activation of calorigenesis in rat brown adipose tissue (BAT), whether mediated by noradrenaline (NA, norepinephrine) released at sympathetic nerve terminals in BAT during cold exposure or by systematically infused NA, is associated with large increases in blood flow (Q) to satisfy the tissue''s O2 requirements. The calorigenic response of BAT to infused NA is a direct function of the steady-state concentration of plasma NA attained during infusion. Whether or not the vasodilation necessary for the calorigenic response is regulated by NA was examined by determining with NA-infused, cold-acclimated rats the effects on calorigenic response and QBAT of artificially changing the concentration of O2 in arterial blood (AO2) by hemodilution, hemoconcentration, or lowering O2 in inspired air. The treatments cause increases or decreases in QBAT without corresponding changes in the rats'' calorigenic response to the NA, in the O2 consumption of interscapular BAT, or in the concentration of plasma NA. The very low QBAT of saline-infused rats was not significantly altered by lowering AO2. QBAT was not directly regulated by the concentration of NA acting on the tissue and AO2, but was adjusted to meet (in only slight excess) the tissue''s O2 requirements. Vasodilation during calorigeneis in BAT may be regulated by some unidentified substance, the production of which is linked to the O2 requirements of the adipocytes, as perhaps sensed through intracellular P[partial pressure]O2. The function of the extensive, vascular, adrenergic innervation of BAT is undetermined.