Inhibition of the sarcolemmal Ca2+ pump in embryonic chick heart cells by mini-glucagon

Sauvadet, Anne; Pecker, Françoise; Pavoine, Catherine

doi:10.1016/0143-4160(95)90047-0

Cited by 11 publications

(11 citation statements)

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“…Cells were then washed two times with saline buffer B and allowed to incubate in the same buffer for 15 min at 25°C to facilitate hydrolysis of intracellular Fura-2/AM. The concentration of Fura-2 in myocytes was estimated as described previously (5,6,21,22) according to the procedure of Donnadieu et al (23). Under usual loading conditions, the average intracellular concentration of Fura-2 was 15 M. Ca 2ϩ imaging was essentially performed as described by Sauvadet et al (6,21).…”

Section: Methodsmentioning

confidence: 99%

“…The concentration of Fura-2 in myocytes was estimated as described previously (5,6,21,22) according to the procedure of Donnadieu et al (23). Under usual loading conditions, the average intracellular concentration of Fura-2 was 15 M. Ca 2ϩ imaging was essentially performed as described by Sauvadet et al (6,21). Field electrical stimulation (square waves, 10-ms duration, amplitude 20% above threshold, and 0.5 Hz) was supplied through a pair of platinum electrodes connected to the output of a HAMEG stimulator.…”

Section: Methodsmentioning

confidence: 99%

“…Primary monolayer cultured heart cells were prepared from 13-day-old embryonic chick ventricles as previously described (5,6,21,22). Briefly, cells were dissociated by repeated cycles of trypsinization.…”

Section: Methodsmentioning

confidence: 99%

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β2-Adrenergic Receptor Agonists Increase Intracellular Free Ca2+ Concentration Cycling in Ventricular Cardiomyocytes through p38 and p42/44 MAPK-mediated Cytosolic Phospholipase A2 Activation

Magne

Couchie

Pecker

et al. 2001

Journal of Biological Chemistry

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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β2-Adrenergic Receptor Agonists Increase Intracellular Free Ca2+ Concentration Cycling in Ventricular Cardiomyocytes through p38 and p42/44 MAPK-mediated Cytosolic Phospholipase A2 Activation

Magne

Couchie

Pecker

et al. 2001

Journal of Biological Chemistry

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“…Primary monolayer cultured heart cells were prepared from 13-day-old chick embryo ventricles as described previously (15,21,22). Briefly, cells were dissociated by repeated cycles of trypsinization.…”

Section: Methodsmentioning

confidence: 99%

“…Cells were then washed with saline buffer B (2 ϫ 2 ml) and allowed to incubate in the same buffer for 15 min at 25°C to facilitate hydrolysis of intracellular Fura-2/AM. The concentration of Fura-2 in myocytes was estimated as described previously (15,21,22), according to the procedure of Donnadieu et al (23). Under usual loading conditions, the average intracellular concentration of Fura-2 was 15 M. Ca 2ϩ imaging, developed by A. Trautman in collaboration with the IMSTAR (Paris, France), was essentially as described by Sauvadet et al (21).…”

Section: Methodsmentioning

confidence: 99%

Evidence for a β2-Adrenergic/Arachidonic Acid Pathway in Ventricular Cardiomyocytes

Pavoine

Magne

Sauvadet

et al. 1999

Journal of Biological Chemistry

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The signaling pathway mediating the contractile effect of ␤ 2 -adrenergic receptors (␤ 2 -AR) in the heart is still matter of debate. By using embryonic chick ventricular cardiomyocytes that express both functional ␤ 1 -and ␤ 2 -ARs, we show here that the specific ␤ 2 -AR agonist, zinterol, increases the amplitude of Ca 2؉ transients and cell contraction of electrically stimulated cells. Zinterol, up to 10 M, did not stimulate adenylyl cyclase activity, and its effect on Ca ␤ 1 -and ␤ 2 -Adrenergic receptors (␤ 1 -and ␤ 2 -ARs) 1 coexist in the hearts of various animal species, including humans. However, their relative amount and their respective participation in the positive chronotropic and inotropic effects of adrenaline and noradrenaline vary depending on the cardiac tissue, the animal species, and/or the pathophysiological state (1, 2). In the non-failing human left ventricle, ␤ 1 -ARs represent 80% of the total ␤-ARs but mediate about 60% only of ␤-adrenergicinduced ventricular contractility (3). In the human failing heart, the ␤ 1 /␤ 2 -AR ratio decreases, and the contribution of ␤ 2 -AR to the contractile responses becomes predominant over that of ␤ 1 -AR, in particular at low adrenaline concentrations (3, 4). For these reasons, the potential role of ␤ 2 -AR for improving cardiac performance has received considerable attention. In fact, the myocardial-targeted overexpression of ␤ 2 -ARs in transgenic mice significantly enhanced myocardial left ventricular contractility (5).It is well documented that ␤ 1 -AR and ␤ 2 -AR subtypes are coupled to adenylyl cyclase activation and that stimulation of both receptors generally leads to an increase in cellular cAMP (4, 6, 7). In human healthy heart, ␤ 2 -ARs are more efficiently coupled to adenylyl cyclase than ␤ 1 -ARs (6 -10). However, during cardiac failure, ␤ 2 -AR subtypes are partially uncoupled from adenylyl cyclase (6, 7), whereas their contribution to the positive inotropic effects of adrenaline and noradrenaline is increased to 63% (7). In addition, studies in the rat heart (11, 12) and in the non-failing and failing canine heart (13) have demonstrated a dissociation between the inotropic effect of ␤ 2 -AR and cellular cAMP increase. Based on those observations, Xiao et al. (12) proposed that unidentified signal transduction pathway(s), other than adenylyl cyclase and cAMP, could be involved in the cardiac inotropic response to ␤ 2 -AR stimulation.Angiotensin II (14,15), bradykinin (16,17), and endothelin (15, 18), which exert positive inotropic responses, evoke AA release in heart. Furthermore, in a recent study, we have demonstrated that glucagon action relies not only on cAMP but also on the synergistic support of AA, by activation of the cPLA 2 which hydrolyzes the sn-2 fatty acyl ester bonds of membranous phospholipids (15).The aim of the present study was to investigate the respective role of cAMP and AA in the cardiac response to ␤-adrenergic agonists. We used the model of embryonic chick ventricular cardiomyocytes that has been widely exploited ...

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Glucagon and Glucagon‐like Peptide Production and Degradation

Kieffer

Hussain

Habener

2001

Comprehensive Physiology

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The sections in this article are: History Glucagon Glucagon‐like Peptides The Glucagon Superfamily of Peptide Hormones Tissue Distribution of Proglucagon Expression Pancreas Intestine Brain Proglucagon Biosynthesis Organization and Structure of the Proglucagon Gene Regulation of Glucagon Gene Expression Posttranslational Processing of Proglucagon Chemistry and Structure Regulation of Glucagon Secretion Overview Intracellular Signals Nutrients Endocrine/Paracrine Neural Pulsatility Regulation of Glucagon‐like Peptide‐1 Secretion Overview Intracellular Signals Nutrients Endocrine Neural Metabolism and Degradation Overview Renal Clearance Hepatic Clearance Degradation in the Circulation Biologically Active Fragments Physiological Actions Glucagon Glucagon‐like Peptide‐1 Glucagon‐like Peptide‐2 Mechanisms of Action Glucagon Glucagon‐like Peptide‐1 Glucagon‐like Peptide‐2 Human Disease Glucagon Glucagon‐like Peptide‐1 Glucagon‐like Peptide‐2

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Inhibition of the sarcolemmal Ca2+ pump in embryonic chick heart cells by mini-glucagon

Cited by 11 publications

References 30 publications

β2-Adrenergic Receptor Agonists Increase Intracellular Free Ca2+ Concentration Cycling in Ventricular Cardiomyocytes through p38 and p42/44 MAPK-mediated Cytosolic Phospholipase A2 Activation

β2-Adrenergic Receptor Agonists Increase Intracellular Free Ca2+ Concentration Cycling in Ventricular Cardiomyocytes through p38 and p42/44 MAPK-mediated Cytosolic Phospholipase A2 Activation

Evidence for a β2-Adrenergic/Arachidonic Acid Pathway in Ventricular Cardiomyocytes

Glucagon and Glucagon‐like Peptide Production and Degradation

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