Perturbation of transmembrane signaling mechanisms in acute and chronic XXXX .

@entity295 @entity5694 @entity8580 @entity7425 @entity141
Our results reviewed here may be summarized as follows: 1. @entity5694 significantly interferes with @entity141 -dependent information flow in the liver. 2. The subcellular sites where these molecular lesions can be localized include: a.) the plasma membrane-there are effects at the level of alpha 1-adrenergic and vasopressin binding, and also in the coupling of receptor activation to @entity8580 lipid metabolism in terms of PIP2 degradation and resynthesis b.) the endoplasmic reticulum in terms of @entity141 release and PI synthesis. Another one of the sequelae of @entity141 -associated receptor activation, namely, cytosolic ionized @entity141 concentration is also affected. 3. Finally, in addition to seeing the impact of acute or continuous @entity5694 at the level of receptor activation and signal generation, we can also document alterations in the expression of physiologic function subserved by these @entity141 - and @entity8580 lipid-associated signaling processes--i.e. in glycogen phosphorylase activity-being consistent with the above described changes. In conclusion, we state that a causal link is shown between receptor binding, agonist-induced @entity7425 hydrolysis, intracellular @entity141 mobilization and activation of phosphorylase a in the liver, suggesting that these alterations may underlie some of the metabolic consequences of chronic @entity295 .
