Constant-pressure perfusion of @entity35 hindlimb shows alpha- and beta-adrenergic stimulation of XXXX consumption.

@entity1169 @entity4962 @entity3159 @entity26 @entity1951 @entity3044 @entity18635 @entity2647 @entity35 @entity1063
Isolated @entity35 hindlimbs were perfused at 37 degrees C and constant physiological pressure (80 +/- 0.5 mmHg) while the flow rate that was allowed to freely self-adjust was monitored. Under these conditions, evidence was obtained for both alpha- and beta-adrenergic stimulation of @entity26 consumption ( @entity4962 ) in contrast to constant-flow perfusion, which has only convincingly shown alpha-adrenergic stimulation of @entity4962 in response to adrenergic agents. Addition of @entity1063 (NE; 1-33 nM) led to an increase in @entity4962 with a maximum of 29% above the basal value at 3.3 nM, even though the flow rate decreased. @entity2647 (3.3-33 nM) and @entity1951 (10-100 pM) also showed similar, but lesser in magnitude, vasoconstriction-associated stimulatory effects on @entity4962 . @entity3159 (an alpha 1-antagonist) completely reversed the NE-mediated decrease in flow rate and significantly blocked the increased @entity4962 . In contrast, @entity3044 (10-1,000 nM) increased both flow rate (30%) and @entity4962 (32%). The @entity3044 -stimulated @entity4962 was not blocked by the beta 1-, beta 2-antagonist @entity1169 (10 microM), although the increased flow was reversed. In the presence of @entity1169 (1 or 10 microM), BRL-35135A (a beta 3-agonist) also stimulated @entity4962 (18%) without significant change in flow rate. These results lend further support to the role of the alpha 1-adrenoceptor in muscle @entity4962 . In addition there is evidence for the presence of a functional @entity18635 as an additional subtype responsible for NE-mediated thermogenesis in the @entity35 hindlimb.
