Epinephrine-stimulated influx

Epinephrine-stimulated Ca2 influx. Our results with D2O also provided evidence that a different platelet agonist i.e. epinephrine, does not act through the same mechanism of Ca2 mobilization as does ADP. In this regard, D2O was not found to be effective in blocking epinephrine-induced platelet activation (29). Therefore, we investigated the possibility that epinephrine, in contrast to ADP, increases platelet membrane permeability to Ca2. Using trace amounts of 45Ca it was demonstrated that epinephrine does in fact induce a transmembrane Ca2 influx which is concomitant with the... 

BAT, in its cold/epinephrine-activated state compared to an atrophied or quiescent state, demonstrates increases in blood flow, lipoprotein lipase activity, triacylglycerol synthesis, 5 -deiodinase activity, and triiodothyronine-enhanced UCP gene expression. The processes of fatty acid uptake and triacylglycerol synthesis are essentially the same in both BAT and WAT. However, norepinephrine release by the sympathetic nervous system in acute cold exposure stimulates BAT to enhance expression and secretion of lipoprotein lipase to its sites in the vascular epithelium. Lipoprotein lipase releases fatty acids from passing chylomicrons and very low-density lipoproteins (Chapter 20), causing an influx of fatty acids into the brown adipocytes. 

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