In a rat model of L-NAME-induced hypertension, beta-blocker therapy, particularly nebivolol, significantly reduced the erythrocyte aggregation index compared to untreated hypertensive controls (p<0.01).
Do beta-blockers improve hemorheological parameters, nitric oxide bioavailability, and oxidative stress in experimental arterial hypertension?
Beta-blockers, particularly nebivolol, partially reverse hemorheological and oxidative stress disturbances in experimental arterial hypertension.
Absolute Event Rate: 46% vs 60%
p-value: p=<0.01
Abstract Background: Arterial hypertension is a multifactorial disorder involving elevated blood pressure, microcirculatory and hemorheological disturbances, endothelial dysfunction, and oxidative stress, which contribute to increased peripheral resistance and disease progression. In this study, we aimed to evaluate the effects of β-blockers on hemorheological parameters, nitric oxide bioavailability, and oxidative stress in experimental arterial hypertension. Methods: Experimental hypertension was induced in male Wistar rats using NG-nitro-L-arginine methyl ester (L-NAME, 40 mg/kg/day). Animals were divided into control, hypertensive, and treatment groups receiving nebivolol, propranolol, metoprolol, or carvedilol. Blood pressure, hemorheological parameters, nitric oxide levels, and total antioxidant activity were evaluated. Results: L-NAME administration significantly increased arterial pressure, erythrocyte aggregation, and plasma viscosity, accompanied by reduced NO levels and decreased antioxidant capacity (p < 0. 01). β-blocker treatment significantly reduced arterial pressure in all groups. Under the present experimental conditions, nebivolol was associated with the greatest improvement in NOx levels, antioxidant activity, and erythrocyte aggregation. However, because equipotent β-blocker dosing was not established, direct comparisons of efficacy among agents should be interpreted cautiously. Carvedilol demonstrated moderate effects, while propranolol and metoprolol showed less improvement in parameters. β-blocker treatment was associated with simultaneous reductions in pulse arterial pressure and erythrocyte aggregation; however, no formal correlation analysis was performed. Conclusions: Experimental hypertension is associated with disturbances in the microcirculation–hemorheology–oxidative stress axis. β-blockers partially reverse these alterations, with nebivolol being associated with more pronounced improvement under the conditions of the present study, likely related, at least in part, to its nitric oxide-mediated and antioxidant properties.
Kajaia et al. (Wed,) conducted a other in Experimental arterial hypertension (n=70). Beta-blockers (nebivolol, propranolol, metoprolol, carvedilol) vs. Untreated hypertensive rats (L-NAME 8 weeks) was evaluated on Erythrocyte aggregation index (EAI) (p=<0.01). In a rat model of L-NAME-induced hypertension, beta-blocker therapy, particularly nebivolol, significantly reduced the erythrocyte aggregation index compared to untreated hypertensive controls (p<0.01).