The above results suggest that AVP induces IL-6 induction in murine hearts via the V<sub>1A</sub> receptor-mediated β-arrestin2/ERK<sub>1/2</sub>/NF-κB pathway, thus reveal a novel mechanism of myocardial inflammation in heart failure involving the V<sub>1A</sub>/β-arrestin 2/ERK<sub>1/2</sub>/NF-κB signaling pathway.
Its absolute values were approximately 350 fmol/mg cytosolic protein, and its expression was not changed in heart failure. beta-Arrestin-2 levels were too low to be detectable using the same methods. beta ARK levels as determined by enzymatic activity were approximately 20 fmol/mg cytosolic protein (beta ARK-1 plus beta ARK-2) and thus almost 20-fold lower than those of beta-arrestin. beta ARK levels were increased approximately twofold in heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)