17beta-estradiol antagonizes cardiomyocyte hypertrophy by autocrine/paracrine stimulation of a guanylyl cyclase A receptor-cyclic guanosine monophosphate-dependent protein kinase pathway.

Background: Significant gender-related differences exist in the development of left ventricular hypertrophy (LVH). In addition, administration of 17beta-estradiol (E2) to ovariectomized female mice attenuates the development of LVH, demonstrating an antagonistic role for E2 in this process, although no molecular mechanism has been proposed for this phenomenon.

Methods And Results: E2 attenuated phenylephrine and endothelin-1 induced hypertrophy in neonatal cardiomyocytes, and E2 directly induced atrial natriuretic factor (ANF) expression as assessed by Northern blot, immunocytochemical analyses, and transient transfection assays using ANF promoter deletion fragments.

Cardiac remodeling after myocardial infarction is impaired in IGF-1 deficient mice.

Objective: To obtain more insight in the role of IGF-1 in cardiac remodeling and function after experimental myocardial infarction. We hypothesized that cardiac remodeling is altered in IGF-1 deficient mice, which may affect cardiac function.

Methods: A myocardial infarction was induced by surgical coronary artery ligation in heterozygous IGF-1 deficient mice.

The murine atrial myosin light chain-2 gene: a member of an evolutionarily conserved family of contractile proteins.

Recently the near complete cDNA of the regulatory atrial myosin light chain (MLC-2a) was cloned. The atrial specific isoform has been shown to be a useful molecular marker for cardiac chamber specification. Therefore, the regulatory sequence of the gene will provide clues on cardiomyocyte differentiation and atrial specific transcription regulation.

Nebivolol: a third-generation beta-blocker that augments vascular nitric oxide release: endothelial beta(2)-adrenergic receptor-mediated nitric oxide production.

Background: Nebivolol is a beta(1)-selective adrenergic receptor antagonist with proposed nitric oxide (NO)-mediated vasodilating properties in humans. In this study, we explored whether nebivolol indeed induces NO production and, if so, by what mechanism. We hypothesized that not nebivolol itself but rather its metabolites augment NO production.