Short-Term Esmolol Improves Coronary Artery Remodeling in Spontaneously Hypertensive Rats through Increased Nitric Oxide Bioavailability and Superoxide Dismutase Activity

The aim of this study was to assess the effects of short-term esmolol therapy on coronary artery structure and function and plasma oxidative stress in spontaneously hypertensive rats (SHR). For this purpose, 14-month-old male SHR were treated for 48 hours with esmolol (SHR-E, 300 μg/kg/min). Age-matched untreated male SHR and Wistar Kyoto rats (WKY) were used as hypertensive and normotensive controls, respectively. At the end of intervention we performed a histological study to analyze coronary artery wall width (WW), wall-to-lumen ratio (W/L), and media cross-sectional area (MCSA). Dose-response curves for acetylcholine (ACh) and sodium nitroprusside were constructed. We also assessed several plasma oxidative stress biomarkers, namely, superoxide scavenging activity (SOSA), nitrites, and total antioxidant capacity (TAC). We observed a significant reduction in WW (P<0.001), W/L (P<0.05), and MCSA (P<0.01) and improved endothelium-dependent relaxation (AUCSHR-E=201.2±33versusAUCSHR=97.5±21,P<0.05) in SHR-E compared with untreated SHR; no differences were observed for WW, MCSA, and endothelium-dependent relaxation by ACh at higher concentrations (10−6to 10−4 mol/l) for SHR-E with respect to WKY. SOSA (P<0.001) and nitrite (P<0.01) values were significantly higher in SHR-E than in untreated SHR; however, TAC did not increase after treatment with esmolol. Esmolol improves early coronary artery remodeling in SHR.

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The effect of short-term canola oil ingestion on oxidative stress in the vasculature of stroke-prone spontaneously hypertensive rats

Lipids in Health and Disease ◽

10.1186/1476-511x-10-180 ◽

2011 ◽

Vol 10 (1) ◽

pp. 180 ◽

Cited By ~ 12

Author(s):

Annateresa Papazzo ◽

Xavier Conlan ◽

Louise Lexis ◽

Paul Lewandowski

Keyword(s):

Oxidative Stress ◽

Canola Oil ◽

Spontaneously Hypertensive Rats ◽

Hypertensive Rats ◽

Short Term ◽

Spontaneously Hypertensive

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Short-term esmolol therapy reverts coronary artery dysfunction in spontaneously hypertensive rats through increased nitric oxide bioavailability and superoxide dismutase activity

European Journal of Anaesthesiology ◽

10.1097/00003643-201406001-00142 ◽

2014 ◽

Vol 31 ◽

pp. 52

Author(s):

A. Arnalich ◽

M. C. Gonzalez ◽

L. Condezo-Hoyos ◽

M. J. Delgado-Martos ◽

E. Delgado-Baeza ◽

...

Keyword(s):

Nitric Oxide ◽

Superoxide Dismutase ◽

Coronary Artery ◽

Spontaneously Hypertensive Rats ◽

Superoxide Dismutase Activity ◽

Hypertensive Rats ◽

Short Term ◽

Spontaneously Hypertensive ◽

Nitric Oxide Bioavailability

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Increased inward rectifier K + current of coronary artery smooth muscle cells in spontaneously hypertensive rats; partial compensation of the attenuated endothelium‐dependent relaxation via Ca 2+ ‐activated K + channels

Clinical and Experimental Pharmacology and Physiology ◽

10.1111/1440-1681.13168 ◽

2019 ◽

Vol 47 (1) ◽

pp. 38-48

Author(s):

Hae Jin Kim ◽

Ming Zhe Yin ◽

Suhan Cho ◽

Sung Eun Kim ◽

Seong Woo Choi ◽

...

Keyword(s):

Smooth Muscle ◽

Coronary Artery ◽

Spontaneously Hypertensive Rats ◽

Inward Rectifier ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

K Channels ◽

K Current ◽

Endothelium Dependent Relaxation ◽

Partial Compensation

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Exercise training improves aortic endothelium-dependent vasorelaxation and determinants of nitric oxide bioavailability in spontaneously hypertensive rats

Journal of Applied Physiology ◽

10.1152/japplphysiol.01252.2003 ◽

2004 ◽

Vol 96 (6) ◽

pp. 2088-2096 ◽

Cited By ~ 77

Author(s):

Drew A. Graham ◽

James W. E. Rush

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Exercise Training ◽

Spontaneously Hypertensive Rats ◽

No Synthase ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Protein Levels ◽

Endothelial No Synthase ◽

Endothelium Dependent Relaxation

The present study examined in vitro vasomotor function and expression of enzymes controlling nitric oxide (NO) bioavailability in thoracic aorta of adult male normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) that either remained sedentary (Sed) or performed 6 wk of moderate aerobic exercise training (Ex). Training efficacy was confirmed by elevated maximal activities of both citrate synthase ( P = 0.0024) and β-hydroxyacyl-CoA dehydrogenase ( P = 0.0073) in the white gastrocnemius skeletal muscle of Ex vs. Sed rats. Systolic blood pressure was elevated in SHR vs. WKY ( P < 0.0001) but was not affected by Ex. Despite enhanced endothelium-dependent relaxation to 10-8 M ACh in SHR vs. WKY ( P = 0.0061), maximal endothelium-dependent relaxation to 10-4 M ACh was blunted in Sed SHR (48 ± 12%) vs. Sed WKY (84 ± 6%, P = 0.0067). Maximal endothelium-dependent relaxation to 10-4 M ACh was completely restored in Ex SHR (93 ± 9%) vs. Sed SHR ( P = 0.0011). Nω-nitro-l-arginine abolished endothelium-dependent relaxation in all groups ( P ≤ 0.0001) and caused equal vasocontraction to maximal ACh in Sed SHR and Ex SHR. Endothelium-independent relaxation to sodium nitroprusside was similar in all groups. Protein levels of endothelial NO synthase were higher in SHR vs. WKY ( P = 0.0157) and in Ex vs. Sed ( P = 0.0536). Protein levels of the prooxidant NAD(P)H oxidase subunit, gp91phox, were higher in SHR vs. WKY ( P < 0.0001) and were diminished in Ex vs. Sed ( P = 0.0557). Levels of the antioxidant SOD-1, -2, and catalase enzymes were lower in SHR vs. WKY (all P ≤ 0.0005) but were not altered by Ex. Thus elevated gp91phox-dependent oxidative stress and reduced antioxidant capacity likely contributed to impaired endothelium-dependent vasorelaxation in Sed SHR. Furthermore, reduced gp91phox-dependent oxidative stress and enhanced endothelial NO synthase-derived NO likely contributed to restored endothelium-dependent vasorelaxation in Ex SHR.

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