PRO-INFLAMMATORY INTERLEUKINS AND OXIDATIVE IMBALANCE IN L-NAME-INDUCED HYPERTENSION: COMPARATIVE EFFECTS OF Β-BLOCKERS.

BACKGROUND

Hypertension is a multifactorial condition characterized by vascular dysfunction, oxidative stress, and immune activation. Pro-inflammatory cytokines, particularly IL-6, IL-17, and TNF-α, contribute to inflammatory processes in hypertension; therefore, they should be considered together with nitric oxide (NO) deficiency and oxidative imbalance when interpreting arterial pressure changes.

OBJECTIVE

To evaluate the association between pro-inflammatory interleukins, nitric oxide metabolites, oxidative status, and arterial pressure in an experimental model of hypertension, and to compare the effects of β-blockers.

METHODS

Hypertension was induced in 70 male Wistar rats by chronic administration of Nω-nitro-L-arginine methyl ester (L-NAME, 40 mg/kg/day, intraperitoneally) for 8 weeks. Animals were randomized into seven groups (n = 10/group): intact control, L-NAME for 4 weeks, L-NAME for 8 weeks, and four L-NAME + β-blocker treatment groups receiving nebivolol (0.5 mg/kg/day), propranolol (0.1 mg/kg/day), metoprolol (3 mg/kg/day), or carvedilol (2 mg/kg/day) by oral gavage during weeks 5-8. Arterial pressure was measured using a noninvasive tail-cuff method. Serum IL-6, IL-17, and TNF-α were quantified by ELISA. Nitric oxide metabolites and total antioxidant activity (TAA) were assessed using the Griess reaction and DPPH assay.

RESULTS

L-NAME administration resulted in a time-dependent increase in arterial pressure, accompanied by reduced NO metabolites and TAA and increased interleukin levels. β-blockers attenuated these changes to varying degrees. Nebivolol and carvedilol produced greater improvements in arterial pressure, NO metabolites, TAA, and interleukin levels compared with propranolol and metoprolol.

CONCLUSION

Chronic NOS inhibition was associated with hypertension and concurrent alterations in inflammatory and oxidative parameters. β-blockers differ in their modulatory effects, with nebivolol and carvedilol demonstrating greater overall efficacy. These findings reflect associations rather than causal mechanisms and support further investigation into integrated therapeutic strategies.