Evidence against noradrenergic regulation of vasodilation in rat brown adipose tissue

In vivo activation of calorigenesis in rat brown adipose tissue (BAT), whether mediated by noradrenaline (NA) released at sympathetic nerve terminals in BAT during cold exposure or by systemically 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 also 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. These treatments resulted in marked 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. Yet the very low QBAT of saline-infused rats was not significantly altered by lowering AO2. Thus QBAT was directly regulated neither by the concentration of NA acting of the tissue nor by AO2, but was adjusted to meet (in only slight excess) the tissue's O2 requirements. This suggests that vasodilation during calorigenesis in BAT is regulated by some as yet unidentified substance, the production of which is linked to the O2 requirements of the adipocytes as perhaps sensed through intracellular PO2. If so, there arises the question of the function of the extensive, vascular, adrenergic innervation of BAT.