Induction of nitric oxide release with nebivolol may improve endothelial dysfunction in polycystic kidney disease

Abstract

To the Editor: We read with great interest the article by Lorthioir et al.1 in which they report that polycystin deficiency induces dopamine-reversible alterations in flowmediated dilatation and vascular nitric oxide release in autosomal-dominant polycystic kidney disease (ADPKD) patients. These patients display a loss of nitric oxide release and an associated reduction in endothelium-dependent dilatation of conduit arteries during sustained blood flow increase. In addition, they suggested that the correction of these anomalies by dopamine could reduce the occurrence of cardiovascular events in ADPKD. Cardiovascular problems due to hypertension are the major cause of morbidity and mortality in patients with ADPKD.2 Recently, it has been shown that oxidative stress and early arterial stiffness are evident in normotensive ADPKD patients.3 Endothelium-dependent relaxation is impaired and endothelial nitric oxide synthase activity is decreased in patients with ADPKD, and endothelial dysfunction secondary to impaired release of nitric oxide exists in these patients. An imbalance in endothelium-derived vasoactive mediators such as nitric oxide might contribute to the pathogenesis of hypertension in ADPKD.2 Nebivolol, a beta-blocker agent, which is associated with the release of nitric oxide, might be useful in ADPKD patients in addition to its favorable effect on blood pressure and endothelial dysfunction.4 Moreover, currently there is no study to show whether nebivolol prevents endothelial dysfunction or not in ADPKD patients. Thus, we propose that it might be plausible to focus on the use of nebivolol in this population to improve endothelial dysfunction.