RT Journal Article
SR Electronic
T1 MECHANISM OF ANTILIPOLYTIC EFFECTS OF CARDIAC GLYCOSIDES
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 284
OP 290
VO 177
IS 1
A1 DAI HYON YU
A1 SHARON TRIESTER
A1 M. I. GLUCKMAN
YR 1971
UL http://jpet.aspetjournals.org/content/177/1/284.abstract
AB The effects of cardiac glycosides (CG) and K+ on norepinephrine (NE)-, theophylline (T)-and dibutyryl cyclic adenosune monophosphate (DB-AMP)-activated lipolysis in rat epididymal fat pads were investigated. Also, theophyllune-unhibited phosphodiesterase activity and the uptake of 3H-NEwere studied. Digitoxin, ouabain and strophanthin-K, as well as K+-free medium, were found to markedly reduce NE-induced glycerol release and to moderately inhibit 3H-NE uptake. It was noted, however, that these inhibitory effects were antagonized by high K+ concentrations. Glycerol release stimulated by T or DB-AMP also was decreased by both CG and lack of K+ whereas theophylline-inhibited phosphodiesterase activity was not influenced by CG. The inhibitory effects of CG on the lipolytic action of T and DB-AMP were antagonized by high K+ and this suggests that the inhibition of glycerol release by CG may involve the cell membrane. Thus, from the above evidence it appears that CG exert their antilipolytic effects by altering the membrane function which results in an inhibition of NE uptake as well as glycerol release caused by NE, T and DB-AMP. Further, the data suggest that K+ coupling is necessary for NE uptake and glycerol release through the cell membrane. © 1971, by The Williams & Wilkins Company