Does nitric oxide inhibit the positive inotropic response to beta-adrenergic stimulation in humans with left ventricular dysfunction?
Nitric oxide produced in the heart attenuates the positive inotropic response to beta-adrenergic stimulation in humans with LV dysfunction. NO may contribute to beta-adrenergic hyporesponsiveness in patients with LV dysfunction.
1α,25-Dihydroxyvitamin D3 attenuates platelet activation and the expression of VCAM-1 and MT1-MMP in human endothelial cells and could have early therapeutic relevance in atherosclerotic diseases.