Alterations in atrial natriuretic peptide gene expression during endurance training in rats

Azizi, Chafik; Bouissou, P.; Galen, F. X.; Lattion, Anne-Laure; Lartigue, M; Carayon, A.

doi:10.1530/eje.0.1330361

Cited by 11 publications

(12 citation statements)

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“…Previous reports on the effect of training on the expression of ANF by ventricular tissue are in conflict. ANF mRNA levels were found to be increased by a rat swim training program (3), a dog treadmill training program (15), and a mouse voluntary wheel running program (1), but unchanged by a treadmill training program in rats (2,12). Because of this uncertainty, we verified the results of our microarray analysis for ANF using RT-PCR and confirmed that ANF expression was decreased in trained compared with control tissue.…”

Section: Discussionmentioning

confidence: 58%

Microarray expression analysis of effects of exercise training: increase in atrial MLC-1 in rat ventricles

Diffee

Seversen

Stein

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Previous studies have shown that endurance exercise training increases myocardial contractility. We have previously described training-induced alterations in myocardial contractile function at the cellular level, including an increase in the Ca(2+) sensitivity of tension. To determine the molecular mechanism(s) of these changes, oligonucleotide microarrays were used to analyze the gene expression profile in ventricles from endurance-trained rats. We used an 11-wk treadmill training protocol that we have previously shown results in increased contractility in cardiac myocytes. After the training, the hearts were removed and RNA was isolated from the ventricles of nine trained and nine control rats. With the use of an Affymetrix Rat Genome U34A Array, we detected altered expression of 27 genes. Several genes previously found to have increased expression in hypertrophied myocardium, such as atrial natriuretic factor and skeletal alpha-actin, were decreased with training in this study. From the standpoint of altered contractile performance, the most significant finding was an increase in the expression of atrial myosin light chain 1 (aMLC-1) in the trained ventricular tissue. We confirmed microarray results for aMLC-1 using RT-PCR and also confirmed a training-induced increase in aMLC-1 protein using two-dimensional gel electrophoresis. aMLC-1 content has been previously shown to be increased in human cardiac hypertrophy and has been associated with increased Ca(2+) sensitivity of tension and increased power output. These results suggest that increased expression of aMLC-1 in response to training may be responsible, at least in part, for previously observed training-induced enhancement of contractile function.

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Section: Discussionmentioning

confidence: 58%

Microarray expression analysis of effects of exercise training: increase in atrial MLC-1 in rat ventricles

Diffee

Seversen

Stein

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…Upregulation of these transcripts is considered a highly conserved feature of ventricular hypertrophy (Lee et al, 1988; Dagnino et al, 1992; Buttrick et al, 1994; Nakagawa et al, 1995), but there are contradictory reports in the literature on the correlation of upregulation of natriuretic peptides with physiological hypertrophy that can be induced by various training programs in animals. Some publications report an upregulation (Buttrick et al, 1994; Allen et al, 2001), while some report no change (Azizi et al, 1995; Jin et al, 2000) or downregulation (Diffee et al, 2003) of ANP and/or BNP expression in these animal models. Both natriuretic peptides were shown to function as modulators of cardiac hypertrophy preventing uncontrolled myocardial growth and regulating ventricular remodeling secondary to compensatory hypertrophy (Tsuruda et al, 2002; Gardner, 2003).…”

Section: Discussionmentioning

confidence: 98%

Remodeling of the heart in hypertrophy in animal models with myosin essential light chain mutations

et al. 2014

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Cardiac hypertrophy represents one of the most important cardiovascular problems yet the mechanisms responsible for hypertrophic remodeling of the heart are poorly understood. In this report we aimed to explore the molecular pathways leading to two different phenotypes of cardiac hypertrophy in transgenic mice carrying mutations in the human ventricular myosin essential light chain (ELC). Mutation-induced alterations in the heart structure and function were studied in two transgenic (Tg) mouse models carrying the A57G (alanine to glycine) substitution or lacking the N-terminal 43 amino acid residues (Δ43) from the ELC sequence. The first model represents an HCM disease as the A57G mutation was shown to cause malignant HCM outcomes in humans. The second mouse model is lacking the region of the ELC that was shown to be important for a direct interaction between the ELC and actin during muscle contraction. Our earlier studies demonstrated that >7 month old Tg-Δ43 mice developed substantial cardiac hypertrophy with no signs of histopathology or fibrosis. Tg mice did not show abnormal cardiac function compared to Tg-WT expressing the full length human ventricular ELC. Previously reported pathological morphology in Tg-A57G mice included extensive disorganization of myocytes and interstitial fibrosis with no abnormal increase in heart mass observed in >6 month-old animals. In this report we show that strenuous exercise can trigger hypertrophy and pathologic cardiac remodeling in Tg-A57G mice as early as 3 months of age. In contrast, no exercise-induced changes were noted for Tg-Δ43 hearts and the mice maintained a non-pathological cardiac phenotype. Based on our results, we suggest that exercise-elicited heart remodeling in Tg-A57G mice follows the pathological pathway leading to HCM, while it induces no abnormal response in Tg-Δ43 mice.

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“…However, it has not been reported whether this also applies to particulate guanylyl cyclase natriuretic peptide receptors in the heart. By contrast, chronic exercise training is generally not associated with elevated plasma ANP levels (Miller et al 1990; Rogers et al 1991; Azizi et al 1995) and the activity of natriuretic peptide receptors are unchanged in adrenal, kidney and lung (Suda et al 2000). Again, no information is available on natriuretic peptide receptors in exercise‐trained hearts.…”

Section: Discussionmentioning

confidence: 99%

Vagal reflex actions of atrial natriuretic peptide survive physiological but not pathological cardiac hypertrophy in rat

Hood

Woods

2004

Experimental Physiology

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Atrial natriuretic peptide (ANP) enhances cardiac vagal baroreflexes in normotensive animals. In spontaneously hypertensive rats (SHRs) this effect of ANP was absent. The reflex actions of ANP were preserved if hypertrophy was completely prevented in SHRs. However even a small amount of cardiac hypertrophy, with no hypertension, in SHRs was accompanied by a loss of the reflex bradycardic actions of ANP. In the present study, we investigated whether pathophysiological cardiac hypertrophy, induced by one-kidney, one-clip renovascular hypertension (1K-1C; n = 6), or physiological cardiac hypertrophy induced by chronic spontaneous, wheel-running exercise training (n = 7), similarly prevented vagal reflex actions of ANP. Cardiac baroreceptor-activated bradycardia was measured during rapid ramp increases (∼5 s) in blood pressure after bolus doses of methoxamine or vehicle in conscious, chronically instrumented rats during infusions of ANP (50 pmol kg −1 min −1 ). Compared with uninephrectomised control rats (n = 10), rats with 1K-1C had cardiac hypertrophy (∼55% increase in left ventricle:body weight (LV:BW) ratio; P < 0.05) and blunted vagal baroreflex gain (−0.93 ± 0.18 versus −0.50 ± 0.13 beats min −1 mmHg −1 ; P < 0.05). ANP did not augment baroreflex function in 1K-1C. Compared with their sedentary controls (n = 7), exercise-trained rats with cardiac hypertrophy (∼20% increase LV:BW ratio; P < 0.05) also had blunted ramp baroreflex bradycardia (−1.28 ± 0.23 versus −0.57 ± 0.09 beats min −1 mmHg −1 ; P < 0.05). In contrast, ANP more than doubled baroreflexbradycardiainexercise-trained rats(P < 0.05).The aetiologyof cardiachypertrophy therefore influenced whether ANP retained its vagal baroreflex enhancing properties.

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Alterations in atrial natriuretic peptide gene expression during endurance training in rats

Cited by 11 publications

References 0 publications

Microarray expression analysis of effects of exercise training: increase in atrial MLC-1 in rat ventricles

Microarray expression analysis of effects of exercise training: increase in atrial MLC-1 in rat ventricles

Remodeling of the heart in hypertrophy in animal models with myosin essential light chain mutations

Vagal reflex actions of atrial natriuretic peptide survive physiological but not pathological cardiac hypertrophy in rat

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