Left ventricular hypertrophy induced by aortic banding impairs relaxation of isolated coronary arteries

McGoldrick, Rory; Kingsbury, Martyn; Turner, Mark A.; Sheridan, Desmond J.; Hughes, Alun D.

doi:10.1042/cs20070136

Cited by 16 publications

(13 citation statements)

References 22 publications

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“…Previous studies have reported that aortic banding causes a number of neuroendocrine changes, including elevated levels of catecholamines, natriuretic peptides, ET-1, and tumor necrosis factor-a, and inconsistently, activation of the renin-angiotensin system. 21 Treatment of aortic-banded animals with the selective SUR2B/Kir6.1 channel opener natakalim restored endothelial function in pressure-overloaded animals.…”

Section: Endothelial Dysfunction In Myocardial Hypertrophymentioning

confidence: 98%

“…20 Some investigators reported that pressure overload-induced LVH causes impaired relaxation of small coronary arteries to endotheliumdependent relaxants and impairment of both the coronary blood flows as a consequence of endothelial dysfunction. 21 Selective impairment of the large coronary artery endothelial function occurred with morphological abnormalities of the endothelium after chronic coronary pressure overload. 19 The endothelium plays a key role in regulating vascular and organ functions through diverse signaling pathways.…”

Section: Endothelial Dysfunction In Myocardial Hypertrophymentioning

confidence: 99%

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Activation of SUR2B/Kir6.1 Subtype of Adenosine Triphosphate-sensitive Potassium Channel Improves Pressure Overload-induced Cardiac Remodeling via Protecting Endothelial Function

Tang¹,

Long²,

Wang³

et al. 2010

Journal of Cardiovascular Pharmacology

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We sought to explore new strategies targeting SUR2B/Kir6.1, a subtype of adenosine triphosphate (ATP)-sensitive potassium channels (KATP), against pressure overload-induced heart failure. The effects of natakalim, a SUR2B/Kir6.1 selective channel opener, on progression of cardiac remodeling were investigated. Pressure overload-induced heart failure was induced in Wistar rats by abdominal aortic banding. The effects of natakalim (1, 3, and 9 mg·kg⁻¹·d⁻¹ for 10 weeks) on myocardial hypertrophy and heart failure, cardiac histology, vasoactive compounds, and gene expression were assessed. Ten weeks after the onset of pressure overload, natakalim treatment potently inhibited cardiac hypertrophy and prevented heart failure. Natakalim remarkably inhibited the changes of left ventricular hemodynamic parameters and reversed the increase of heart mass index, left ventricular weight index, and lung weight index. Histological examination demonstrated that there was no significant hypertrophy or fibrosis in pressure-overloaded hearts of natakalim-treated rats. Ultrastructural examination of hearts revealed well-organized myofibrils with mitochondria grouped along the periphery of longitudinally oriented fibers in rats from the natakalim group. The content of serum nitric oxide and plasma prostacyclin was increased, whereas that of plasma endothelin-1 and cardiac tissue hydroxyproline and atrial and B-type natriuretic peptide messenger RNA was downregulated in natakalim-treated rats. Natakalim at 0.01-100 µM had no effects on isolated working hearts derived from Wistar rats; however, natakalim had endothelium-dependent vasodilatory effects on the isolated tail artery helical strips precontracted with norepinephrine. These results indicate that natakalim reduces heart failure caused by pressure overloading by activating the SUR2B/Kir6.1 KATP channel subtype and protecting against endothelial dysfunction.

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Section: Endothelial Dysfunction In Myocardial Hypertrophymentioning

confidence: 98%

Section: Endothelial Dysfunction In Myocardial Hypertrophymentioning

confidence: 99%

Activation of SUR2B/Kir6.1 Subtype of Adenosine Triphosphate-sensitive Potassium Channel Improves Pressure Overload-induced Cardiac Remodeling via Protecting Endothelial Function

Tang¹,

Long²,

Wang³

et al. 2010

Journal of Cardiovascular Pharmacology

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“…; McGoldrick et al . ). Heart‐to‐body weight ratio, the commonly used index of cardiac hypertrophy, indicates that significant hypertrophy (an increase of around 50%) has developed by this time (similar in extent to that found by Kingsbury et al .…”

Section: Discussionmentioning

confidence: 97%

Changes in cellular Ca²⁺ and Na⁺ regulation during the progression towards heart failure in the guinea pig

Yang

Francis

et al. 2019

The Journal of Physiology

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Key points During compensated hypertrophy in vivo fractional shortening (FS) remains constant until heart failure (HF) develops, when FS decreases from 70% to 39%. Compensated hypertrophy is accompanied by an increase in INa,late and a decrease in Na+,K+‐ATPase current. These changes persist as HF develops. SR Ca2+ content increases during compensated hypertrophy then decreases in HF. In healthy cells, increases in SR Ca2+ content and Ca2+ transients can be achieved by the same amount of inhibition of the Na+,K+‐ATPase as measured in the diseased cells. SERCA function remains constant during compensated hypertrophy then decreases in HF, when there is also an increase in spark frequency and spark‐mediated Ca2+ leak. We suggest an increase in INa,late and a decrease in Na+,K+‐ATPase current and function alters the balance of Ca2+ flux mediated by the Na+/Ca2+ exchange that limits early contractile impairment. Abstract We followed changes in cardiac myocyte Ca2+ and Na+ regulation from the formation of compensated hypertrophy (CH) until signs of heart failure (HF) are apparent using a trans‐aortic pressure overload (TAC) model. In this model, in vivo fractional shortening (FS) remained constant despite HW:BW ratio increasing by 39% (CH) until HF developed 150 days post‐TAC when FS decreased from 70% to 39%. Using live and fixed fluorescence imaging and electrophysiological techniques, we found an increase in INa,late from –0.34 to –0.59 A F−1 and a decrease in Na+,K+‐ATPase current from 1.09 A F−1 to 0.54 A F−1 during CH. These changes persisted as HF developed (INa,late increased to –0.82 A F−1 and Na+,K+‐ATPase current decreased to 0.51 A F−1). Sarcoplasmic reticulum (SR) Ca2+ content increased during CH then decreased in HF (from 32 to 15 μm l−1) potentially supporting the maintenance of FS in the whole heart and Ca2+ transients in single myocytes during the former stage. We showed using glycoside blockade in healthy myocytes that increases in SR Ca2+ content and Ca2+ transients can be driven by the same amount of inhibition of the Na+,K+‐ATPase as measured in the diseased cells. SERCA function remains constant in CH but decreases (τ for SERCA‐mediated Ca2+ removal changed from 6.3 to 3.0 s−1) in HF. In HF there was an increase in spark frequency and spark‐mediated Ca2+ leak. We suggest an increase in INa,late and a decrease in Na+,K+‐ATPase current and function alters the balance of Ca2+ flux mediated by the Na+/Ca2+ exchange that limits early contractile impairment.

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“…One of the advantages of this model is that the contralateral side can be used as a normotensive control. Previous studies found disparate effects of hypertension induced by aortic banding on endothelium-dependent function in aorta or coronary arteries [13, 27], probably due to the differences in the vascular beds studied and the location of the band. In this study, our finding that transverse aortic banding impairs endothelium-dependent dilatation in right-sided (hypertensive) cerebral arterioles in WT mice, but not in Nox2-/y mice, suggests that superoxide derived from Nox2-containing NADPH oxidase may play an important role in altered endothelium-dependent function in cerebral arterioles during hypertension.…”

Section: Discussionmentioning

confidence: 99%

Nox2 Deficiency Prevents Hypertension-Induced Vascular Dysfunction and Hypertrophy in Cerebral Arterioles

Chan

Baumbach

2013

International Journal of Hypertension

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Oxidative stress is involved in many hypertension-related vascular diseases in the brain, including stroke and dementia. Thus, we examined the role of genetic deficiency of NADPH oxidase subunit Nox2 in the function and structure of cerebral arterioles during hypertension. Arterial pressure was increased in right-sided cerebral arterioles with transverse aortic banding for 4 weeks in 8-week-old wild-type (WT) and Nox2-deficient (-/y) mice. Mice were given NG-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg) or vehicle to drink. We measured the reactivity in cerebral arterioles through open cranial window in anesthetized mice and wall cross-sectional area and superoxide levels ex vivo. Aortic constriction increased systolic and pulse pressures in right-sided carotid arteries in all groups of mice. Ethidium fluorescence showed increased superoxide in right-sided cerebral arterioles in WT, but not in Nox2-/y mice. Dilation to acetylcholine, but not sodium nitroprusside, was reduced, and cross-sectional areas were increased in the right-sided arterioles in WT, but were unchanged in Nox2-/y mice. L-NAME reduced dilation to acetylcholine but did not result in hypertrophy in right-sided arterioles of Nox2-/y mice. In conclusion, hypertension-induced superoxide production derived from Nox2-containing NADPH oxidase promotes hypertrophy and causes endothelial dysfunction in cerebral arterioles, possibly involving interaction with nitric oxide.

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Left ventricular hypertrophy induced by aortic banding impairs relaxation of isolated coronary arteries

Cited by 16 publications

References 22 publications

Activation of SUR2B/Kir6.1 Subtype of Adenosine Triphosphate-sensitive Potassium Channel Improves Pressure Overload-induced Cardiac Remodeling via Protecting Endothelial Function

Activation of SUR2B/Kir6.1 Subtype of Adenosine Triphosphate-sensitive Potassium Channel Improves Pressure Overload-induced Cardiac Remodeling via Protecting Endothelial Function

Changes in cellular Ca²⁺ and Na⁺ regulation during the progression towards heart failure in the guinea pig

Nox2 Deficiency Prevents Hypertension-Induced Vascular Dysfunction and Hypertrophy in Cerebral Arterioles

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Left ventricular hypertrophy induced by aortic banding impairs relaxation of isolated coronary arteries

Cited by 16 publications

References 22 publications

Activation of SUR2B/Kir6.1 Subtype of Adenosine Triphosphate-sensitive Potassium Channel Improves Pressure Overload-induced Cardiac Remodeling via Protecting Endothelial Function

Activation of SUR2B/Kir6.1 Subtype of Adenosine Triphosphate-sensitive Potassium Channel Improves Pressure Overload-induced Cardiac Remodeling via Protecting Endothelial Function

Changes in cellular Ca2+ and Na+ regulation during the progression towards heart failure in the guinea pig

Nox2 Deficiency Prevents Hypertension-Induced Vascular Dysfunction and Hypertrophy in Cerebral Arterioles

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Product

Resources

About

Changes in cellular Ca²⁺ and Na⁺ regulation during the progression towards heart failure in the guinea pig