Effect of Training on ??1 ??2 ??3 Adrenergic and M2 Muscarinic Receptors in Rat Heart

Barbier, J.; Rannou-Bekono, Françoise; Marchais, J.; Berthon, Pierre; Delamarche, Paul; Carré, François

doi:10.1249/01.mss.0000128143.93407.39

Cited by 43 publications

(43 citation statements)

References 27 publications

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“…Barbier and colleagues also detected transcripts and cell surface expression of ␤ 3 -AR in rat hearts. They further found that LV ␤ 3 -AR density significantly increased in female rats with treadmill training for 8 weeks (Barbier et al, 2004).…”

Section: Discussionmentioning

confidence: 90%

Enhanced Inhibition of L-type Ca²⁺ Current by β₃-Adrenergic Stimulation in Failing Rat Heart

Zhang

Cheng²,

Onishi³

et al. 2005

J Pharmacol Exp Ther

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␤ 3 -adrenergic receptors (AR) have recently been identified in mammalian hearts and shown to be up-regulated in heart failure (HF). ␤ 3 -AR stimulation reduces inotropic response associated with an inhibition of L-type Ca 2ϩ channels in normal hearts; however, the effects of ␤ 3 -AR activation on Ca 2ϩ channel in HF remain unknown. We compared the effects of ␤ 3 -AR activation on L-type Ca 2ϩ current (I Ca,L ) in isolated left ventricular myocytes obtained from normal and age-matched rats with isoproterenol (ISO)-induced HF (4 months after 340 mg/kg s.c.

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Section: Discussionmentioning

confidence: 90%

Enhanced Inhibition of L-type Ca²⁺ Current by β₃-Adrenergic Stimulation in Failing Rat Heart

Zhang

Cheng²,

Onishi³

et al. 2005

J Pharmacol Exp Ther

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“…This eVect signiWes an important adaptation to training given that cardiac -adrenergic receptor density, as a whole, appears to decline with training. For example, swim training has been reported to down-regulate cardiac -adrenergic receptors without altering the ratio of 1 to 2s subtypes (Barbier et al 2004(Barbier et al , 2006Werle et al 1990). Conversely, a reduction in cardiac 1-adrenergic receptor density following training without an alteration in 2-adrenergic receptor density in female WKY rats has been shown (Barbier et al 2004(Barbier et al , 2006.…”

Section: Discussionmentioning

confidence: 99%

Cardiac β-adrenergic responsiveness with exercise

Libonati

MacDonnell

2011

Eur J Appl Physiol

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Left ventricular performance is enhanced with chronic exercise training. Alterations in cardiomyocyte β-adrenergic responsiveness (BAR) may, in part, mediate this response. In this study, cardiac BAR and the expression of some key cardiac hypertrophic signaling molecules following 3 months of treadmill training were examined. Four-month old, female, Wistar Kyoto (WKY) rats were randomly assigned into either a sedentary (WKY-SED, n = 15) or an exercise-trained (WKY-TRD, n = 11) group. All rats were maintained on a 12-h light/dark cycle, and fed ad libitum. Exercise training consisted of motorized treadmill training at 25 m/min, 0% grade, 60 continuous minutes, 5 days/week for a period of 12 weeks. RT-PCR was used to establish basal cardiac calcineurin A, ANP, and AKT mRNA expression. In vitro cardiac BAR responsiveness was determined in Langendorff, isolated hearts. Following baseline, isoproterenol (ISO) was incrementally infused at concentrations ranging from 1 × 10(-10) to 1 × 10(-7) mol/L. There were no group differences for heart weight, heart to body weight ratio, calcineurin A, ANP, or AKT mRNA levels between WKY-SED and WKY-TRD. WKY-TRD showed enhanced cardiac BAR relative to WKY-SED (at ISO 1 × 10(-7) mol/L; P < 0.05). Moderate intensity treadmill exercise improved cardiac BAR responsiveness to a high concentration of isoproterenol. This adaptation was independent of training-induced alterations in cardiac hypertrophy or hypertrophic marker expression.

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“…In general, cardiac AR density has been shown to decline with exercise training without changing the ratio of AR1 to AR2s subtypes [96][97][98]. Still other studies have shown an attenuation of AR1s with training without altering AR2s.…”

Section: -Adrenergic Responsivenessmentioning

confidence: 95%

Cardiac Effects of Exercise Training in Hypertension

Libonati

2013

ISRN Hypertension

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Hypertension is a signi�cant health concern. Hypertension leads to compensatory pathologic hypertrophy and impaired cardiac function. Lifestyle modi�cations such as exercise are encouraged for hypertensive patients. Some studies have shown that exercise training can reverse pathological hypertrophy. Conversely, studies on animal models of hypertension have shown increased cardiac growth with exercise training. Despite the further induction of hypertrophy, exercise training seems protective against cell death and may increase cardiomyocyte proliferation, leading to a putative phenotype. �ne of the hallmark bene�cial effects of exercise in hypertension is an improvement in myocardial adrenergic responsiveness. e focus of this paper is to discuss how exercise training impacts cardiac remodeling and function in the hypertensive heart with speci�c reference to adrenergic signaling.

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Effect of Training on ??1 ??2 ??3 Adrenergic and M2 Muscarinic Receptors in Rat Heart

Cited by 43 publications

References 27 publications

Enhanced Inhibition of L-type Ca²⁺ Current by β₃-Adrenergic Stimulation in Failing Rat Heart

Enhanced Inhibition of L-type Ca²⁺ Current by β₃-Adrenergic Stimulation in Failing Rat Heart

Cardiac β-adrenergic responsiveness with exercise

Cardiac Effects of Exercise Training in Hypertension

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Effect of Training on ??1 ??2 ??3 Adrenergic and M2 Muscarinic Receptors in Rat Heart

Cited by 43 publications

References 27 publications

Enhanced Inhibition of L-type Ca2+ Current by β3-Adrenergic Stimulation in Failing Rat Heart

Enhanced Inhibition of L-type Ca2+ Current by β3-Adrenergic Stimulation in Failing Rat Heart

Cardiac β-adrenergic responsiveness with exercise

Cardiac Effects of Exercise Training in Hypertension

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Enhanced Inhibition of L-type Ca²⁺ Current by β₃-Adrenergic Stimulation in Failing Rat Heart

Enhanced Inhibition of L-type Ca²⁺ Current by β₃-Adrenergic Stimulation in Failing Rat Heart