The endogenous peptide apelin potently improves cardiac contractility and reduces cardiac loading in vivo

Ashley, Euan A.; Powers, Jennifer; CHEN, M; Kundu, Ramendra K.; Finsterbach, Thomas; Caffarelli, Anthony D.; Deng, Alicia; Eichhorn, Joachim; Mahajan, Raghu; Agrawal, Rani

doi:10.1016/j.cardiores.2004.08.018

Cited by 315 publications

(247 citation statements)

References 30 publications

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“…Network models exhibiting scale-free topology identify disproportionately important roles for highly connected hubs. Hub genes revealed in this way represent attractive targets for biological and therapeutic exploration (29). Here, we took advantage of the availability of human tissue derived from coronary atherectomy to build blood vessel-specific network models identifying GPX1 as a hypothetical mediator of disease.…”

Section: Discussionmentioning

confidence: 99%

Oxido-reductive regulation of vascular remodeling by receptor tyrosine kinase ROS1

et al. 2014

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Section: Discussionmentioning

confidence: 99%

Oxido-reductive regulation of vascular remodeling by receptor tyrosine kinase ROS1

et al. 2014

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“…Functionally, actions of apelin start to emerge as evident in experimental studies (for a review see 3). For example, apelin has been shown to exert cardiovascular effects including positive inotropic action and to reduce blood pressure, as demonstrated in rodents (3,15,16). Apelin also increases drinking behavior (14) and reduces food intake (17) in model experiments in rodents.…”

Section: Introductionmentioning

confidence: 98%

The apj receptor is expressed in pancreatic islets and its ligand, apelin, inhibits insulin secretion in mice

Winzell

Magnusson

Åhrén

2005

Regulatory Peptides

177

114

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Apelin is the endogenous ligand of the G-protein coupled apj receptor. Apelin is expressed in the brain, the hypothalamus and the stomach and was recently shown also to be an adipokine secreted from the adipocytes. Although apelin has been suggested to be involved in the regulation of food intake, it is not known whether the peptide affects islet function and glucose homeostasis. We show here that the apj receptor is expressed in pancreatic islets and that intravenous administration of full-length apelin-36 (2 nmol/kg) inhibits the rapid insulin response to intravenous glucose (1g/kg) by 35% in C57BL/6J mice. Thus, the acute (1-5 min) insulin response to intravenous glucose was 682±23 pmol/l after glucose alone (n=17) and 445±58 pmol/l after glucose plus apelin-36 (n=18; P=0.017). This was associated with impaired glucose elimination (the 5-20 min glucose elimination was 2.9±0.1%/min after glucose alone versus 2.3±0.2%/min after glucose plus apelin-36, P=0.008). Apelin (2nmol/kg) also inhibited the insulin response to intravenous glucose in obese insulin resistant high-fat fed C57BL/6J mice (P=0.041). After 60 min incubation of isolated islets from normal mice, insulin secretion in the presence of 16.7 mmol/l glucose was inhibited by apelin-36 at 1 µmol/l, whereas apelin-36 did not significantly affect insulin secretion at 2.8 or 8.3 mmol/l glucose or after stimulation of insulin secretion by KCl. Islet glucose oxidation at 16.7 mmol/l was not affected by apelin-36. We conclude that the apj receptor is expressed in pancreatic islets and that apelin-36 inhibits glucose-stimulated insulin secretion both in vivo and in vitro.This may suggest that the islet beta-cells are targets for apelin-36.

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“…Apelin increases the contractile force of the myocardium (22)(23)(24), and apelin gene-deficient mice subjected to chronic pressure overload developed severe and progressive heart failure (25). Moreover, intravenous injection of K17F or pE13F in rodents decreases arterial blood pressure (BP) and increases heart rate (7,14,16) via a NO production (26) with a greater effect for K17F than for pE13F (14).…”

mentioning

confidence: 99%

Biased Signaling Favoring Gi over β-Arrestin Promoted by an Apelin Fragment Lacking the C-terminal Phenylalanine

Ceraudo¹,

Galanth²,

Carpentier³

et al. 2014

Journal of Biological Chemistry

103

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Background: Apelin receptor represents a therapeutic target for cardiovascular diseases. Results: Apelin 17 activates ERK1/2 in a ␤-arrestin-dependent and G protein-dependent manner, whereas apelin 17 with deleted C-terminal phenylalanine only signals through the G protein. Conclusion:Biased signaling promoted by an apelin fragment lacking the C-terminal phenylalanine is favoring G i over ␤-arrestin. Significance: Apelin receptor ␤-arrestin signaling may account for apelin hypotensive activity.

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The endogenous peptide apelin potently improves cardiac contractility and reduces cardiac loading in vivo

Abstract: Apelin reduces left ventricular preload and afterload and increases contractile reserve without evidence of hypertrophy. These results associate apelin with a positive hemodynamic profile and suggest it as an attractive target for pharmacotherapy in the setting of heart failure.

Cited by 315 publications

References 30 publications

Oxido-reductive regulation of vascular remodeling by receptor tyrosine kinase ROS1

Oxido-reductive regulation of vascular remodeling by receptor tyrosine kinase ROS1

The apj receptor is expressed in pancreatic islets and its ligand, apelin, inhibits insulin secretion in mice

Biased Signaling Favoring Gi over β-Arrestin Promoted by an Apelin Fragment Lacking the C-terminal Phenylalanine

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