calcimycin and Cardiovascular-Diseases

Nitric oxide synthases (NOSs) are key enzymes regulating vascular function. Previously, we reported that β-adrenergic (β-AR) overstimulation, a common feature of cardiovascular diseases, did not impair endothelium-dependent vasodilation, although it resulted in endothelial NOS (eNOS) uncoupling and reduced NO bioavailability. In addition to NO, neuronal NOS (nNOS) produces H. Male C57BL/6 wild-type and nNOS knockout mice (nNOS. Acetylcholine- or calcium ionophore A23187-induced endothelium-dependent relaxation was similar in aortic rings from VHE and ISO. However, this relaxation was significantly reduced in aortas from ISO compared to VHE when (1) caveolae were disrupted, (2) nNOS was pharmacologically inhibited or genetically suppressed and (3) H. The results suggest a role of caveolin-1 and the nNOS/H

Topics: Adrenergic beta-Agonists; Animals; Calcimycin; Calcium Ionophores; Cardiovascular Diseases; Caveolin 1; Endothelium, Vascular; Hydrogen Peroxide; Isoproterenol; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Nitric Oxide Synthase Type I; Receptors, Adrenergic, alpha; Vasodilation