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Published on: February 25, 2016
Propranolol treatment lowers blood pressure, reduces vascular inflammatory markers and improves endothelial function
Nathalia da Silva Franco1, Camila Lubaczeuski1, Daniele M Guizoni1
1Department of Structural and Functional Biology, Institute of Biology, University of Campinas-UNICAMP, Campinas, Brazil.
Abstract:
Obesity-associated hypertension is accompanied by a number of cardiovascular risk factors including vascular insulin resistance (IR) and higher sympathetic nervous activity. Therefore, autonomic blockade was demonstrated to reverse hypertension, endothelial dysfunction and IR in obese individuals. We hypothesized that β-AR blockade with propranolol would restore endothelial function and vascular insulin signaling in obesity, associated with an anti-inflammatory effect. Body weight, systolic blood pressure (SBP), plasma biochemical parameters and aortic endothelial function were analyzed in mice fed standard diet (control group) or a high fat diet (HFD) that were treated with vehicle (water) or propranolol (10mg/kg/day) for 8weeks. Propranolol treatment did not modify obesogenic effect of HFD feeding. However, propranolol was effective in preventing the rise in SBP, the hyperinsulinemia and the impaired endothelium-dependent relaxation to acetylcholine and to insulin in obese mice. Protective effect of propranolol administration in endothelial function was associated with increased nitric oxide (NO) production and phosphorylation of Akt (Ser473) and eNOS (Ser1177), but with reduced phospho-IRS-1(Ser307) and phospho-ERK1/2 (Thr202/Tyr204). In addition, β-blocker propranolol prevented the NF-kB nuclear translocation and the increase in phospho-IκB-α (Ser32) and in interleukin(IL)-6 expression in aorta of obese mice, without significant changes in either aortic reactive oxygen species production or in circulating IL-6 and TNF-α levels. In β2-AR knockout mice, despite increasing body weight and visceral fat, HFD did not increase SBP and showed a partial improvement of endothelial function, revealing a role of β2-AR in cardiovascular effects of obesity. In conclusion, our results suggest that β-AR blockade with propranolol is effective to prevent the endothelial dysfunction, vascular IR and pro-inflammatory state displayed in HFD-induced obesity, independent of changes in body weight.
Insights
Beta-blocker propranolol prevents obesity-related hypertension, vascular insulin resistance, and inflammation by improving endothelial function. This effect occurs independently of body weight changes in mice.
Area of Science:
- Cardiovascular Physiology
- Metabolic Syndrome Research
- Pharmacology
Background:
- Obesity-associated hypertension involves vascular insulin resistance (IR) and heightened sympathetic activity.
- Autonomic blockade has previously reversed hypertension, endothelial dysfunction, and IR in obese individuals.
- Beta-adrenergic receptor (β-AR) blockade is hypothesized to restore endothelial function and vascular insulin signaling in obesity.
Purpose of the Study:
- To investigate the effects of β-AR blockade with propranolol on endothelial function, vascular insulin signaling, and inflammation in diet-induced obesity.
- To determine if propranolol can prevent or reverse hypertension and endothelial dysfunction in obese mice.
- To elucidate the role of β2-adrenergic receptors in the cardiovascular effects of obesity.
Main Methods:
- Mice were fed a standard diet or a high-fat diet (HFD) and treated with vehicle or propranolol for 8 weeks.
- Measurements included body weight, systolic blood pressure (SBP), plasma biochemistry, and aortic endothelial function.
- Molecular analyses assessed nitric oxide (NO) production, signaling pathway phosphorylation (Akt, eNOS, IRS-1, ERK1/2), NF-κB activation, and inflammatory cytokine expression.
Main Results:
- Propranolol prevented HFD-induced increases in SBP, hyperinsulinemia, and impaired endothelium-dependent relaxation.
- Propranolol enhanced NO production and improved insulin signaling (Akt, eNOS) while reducing inflammation markers (phospho-IRS-1, NF-κB activation, IL-6 expression).
- β2-AR knockout mice showed resistance to HFD-induced hypertension and partial improvement in endothelial function, highlighting β2-AR's role.
Conclusions:
- β-AR blockade with propranolol effectively prevents endothelial dysfunction, vascular IR, and the pro-inflammatory state in diet-induced obesity.
- These beneficial effects are independent of changes in body weight.
- The findings underscore the therapeutic potential of β-AR blockade in managing obesity-related cardiovascular complications.
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