The Aldosterone Receptor Antagonist Eplerenone Inhibits Isoproterenol-Induced Collagen-I and 11β-HSD1 Expression in Rat Cardiac Fibroblasts and the Left Ventricle.

β-Adrenergic receptor (β-AR)-induction of collagen-I synthesis is partially mediated by the cardiac mineralocorticoid receptor (MR) system. However, it remains unclear whether the selective MR antagonist, eplerenone, inhibits collagen-I synthesis induced by β-AR stimulation. We investigated the effects of eplerenone on the responses to a non-selective β-AR agonist, isoproterenol, which induced collagen-I synthesis in primary cardiac fibroblasts (CFs) and the left ventricle.

Matrix metalloproteinase-2 stimulates collagen-I expression through phosphorylation of focal adhesion kinase in rat cardiac fibroblasts.

Collagen-I is thought to be the main component of the extracellular matrix in cardiac fibrosis, the accumulation of which occurs with excessive activation of matrix metalloproteinase-2 (MMP-2). MMP-2 degrades the extracellular matrix; however, the relative importance of MMP-2 to collagen-I synthesis in cardiac fibroblasts remains unclear. We investigated whether extracellular activation of MMP-2 regulates collagen-I synthesis and phosphorylation of focal adhesion kinase (FAK) in rat cardiac fibroblasts.

Diagnostic utility of NT-proBNP and ANP in a canine model of chronic embolic pulmonary hypertension.

The information needed to diagnose pulmonary arterial hypertension (PAH) in dogs based on N-terminal pro B-type natriuretic peptide (NT-proBNP) and atrial natriuretic peptide (ANP) levels is unclear. In this study, serial changes in plasma NT-proBNP and ANP concentrations were evaluated in association with the development of chronic embolic pulmonary hypertension (CEPH). Six Beagle dogs underwent percutaneous pulmonary artery catheterization.

Bioinformatics research on inter-racial difference in drug metabolism I. Analysis on frequencies of mutant alleles and poor metabolizers on CYP2D6 and CYP2C19.

The enzyme activities of CYP2D6 and CYP2C19 show a genetic polymorphism, and the frequency of poor metabolizers (PMs) on these enzymes depends on races. In the present study, the frequencies of mutant alleles and PMs in each race were analyzed based on information from published studies, considering the genetic polymorphisms of CYP2D6 and CYP2C19 as the causal factors of racial and inter-individual differences in pharmacokinetics. As a result, it was shown that there were racial differences in the frequencies of each mutant allele and PMs.