Nitric oxide mediated effects of nebivolol on erectile function in rats with heart failure

Background and objective: Heart failure (HF) is a common complication of cardiovascular disease, which leads to functional cardiac abnormalities. Beta-blockers are commonly used to reduce mortality in HF patients; however, they are associated with an increased risk of erectile dysfunction (ED). Nebivolol is a third-generation beta-blocker with also having a Nitric oxide (NO) releasing effect. NO plays a key role in penile erection. The aim of this study was to investigate the NO-mediated effects of nebivolol on ED in HF. Material and methods: Twenty-four weeks old rats were divided into three groups: sham-operated control (SC), HF-induced control (HFC), and nebivolol-treated (HFNEB). HF was induced by the ligation of the left anterior descending coronary artery. Eight weeks after the ligation, functional, hemodynamic, biologic, and histologic studies were conducted to assess NO-mediated effects of nebivolol. Results: HF rats displayed impaired erectile function represented by decreased intracavernosal/mean arterial pressure ratio (ICP/MAP). Increased nitrosative damage/decreased antioxidant capacity was consistent with decreased endothelial NOS (eNOS) and increased inducible NOS (iNOS) and neuronal NOS (nNOS) immunoreactivity in this group. Nebivolol treated animals were characterized by improved functional capacity, increased antioxidant and decreased oxidant capacity. Prevention of eNOS and an increase in nNOS immunoreactivity was also significant in this group. Conclusion: Our study showed the positive effects of nebivolol on erectile function in HF. NO-mediated mechanisms behind this effect can be summarized as eNOS mediated dilation of the cavernous body and nNOS mediated smooth muscle relaxation. To the best of our knowledge, this study is the first in the literature to discuss all three NOS isoforms in order to explain the NO-mediated effects of nebivolol in ED

Nitric oxide mediated effects of nebivolol in cardiorenal syndrome

Objective(s): Despite several proposed mechanisms for the pathophysiology of cardiorenal syndrome (CRS), the exact mechanism remains unclear. Nitrosative stress has been argued as a key mechanism recently. Nebivolol is a beta-blocker with nitric oxide (NO)-releasing effect. In the present study, NO-mediated effects of two different treatment regimes of nebivolol in CRS were studied

The Effect of Nebivolol on Acute Renal Injury Developed After Myocardial Ischemia: A Preclinical Study

Aim: During reperfusion of myocardial ischemia, damage can also be seen in the kidneys. Although many studies have been conducted on the underlying mechanisms, the basic mechanism of this interaction is still unknown. We think that this is oxidative/nitrosative damage caused by hypoperfusion. Nebivolol is a beta-blocker with nitric oxide (NO)-mediated effects. In this study, we aimed to investigate the NO-mediated effect of nebivolol on acute renal injury (ARI) developed after myocardial ischemia-reperfusion (IR)

The effects of nebivolol on apoptosis in a rat infarct model

Background In the present study, nitric oxide (NO) was investigated to see if it mediated effects of nebivolol on apoptosis in the rat myocardial infarction (MI) model