Apelin activates l-arginine/nitric oxide synthase/nitric oxide pathway in rat aortas

Jia, Yong; Lu, Zheng Fei; Zhang, Jing; Pan, Chun; Yang, Jing; Zhao, Jing; Yu, Fang; Xiao, Duan; Tang, Chao; Qi, Yong

doi:10.1016/j.peptides.2007.07.016

Cited by 104 publications

(76 citation statements)

References 30 publications

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“…These authors showed that apelin-13 decreased production of ROS and malonic dialdehyde (MDA) with a simultaneous increase in superoxide dismutase (SOD) activity in both types of experimental preparations. A similar effect of apelin-13 on MDA formation was previously described in rat aortas by Jia et al [41]. The increased activity of SOD by apelin can remove a large portion of superoxide anion, thereby reducing I/R injury.…”

Section: Discussionsupporting

confidence: 77%

Nitric oxide synthase mediates the apelin-induced improvement of myocardial postischemic metabolic and functional recovery

Писаренко¹,

Pelogeykina²,

Shulzhenko³

et al. 2012

OJMIP

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The adipocytokine apelin is capable to reduce myocardial ischemia/reperfusion injury in rodents. Cardioprotective activity of apelin may be attributed to upregulation of endothelial nitric oxide synthase (eNOS). This study was designed to examine metabolic and functional effects of a synthesized 12 Cterminal residue of apelin (A-12) and N G -nitro-L-arginine methyl ester (L-NAME), a non-selective eNOS inhibitor, in isolated working rat hearts subjected to global ischemia. Preischemic infusion of A-12 increased recovery of cardiac function during reperfusion compared with control and resulted in enhanced restoration of myocardial ATP, adenine nucleotide pool, phosphocreatine and reduction of myocardial lactate and lactate/pyruvate ratio. Coadministration of A-12 and L-NAME aggravated recovery of coronary flow and cardiac function compared with these indices after A-12 treatment. Cardiac dysfunction was associated with increase in lactate dehydrogenase release in myocardial effluent, reduction of glucose oxidation and abolishment of augmented restoration of high energy phosphates. The results clearly demonstrate involvement of NOS-dependent mechanisms in cardioprotection afforded by apelin.

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Section: Discussionsupporting

confidence: 77%

Nitric oxide synthase mediates the apelin-induced improvement of myocardial postischemic metabolic and functional recovery

Писаренко¹,

Pelogeykina²,

Shulzhenko³

et al. 2012

OJMIP

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“…This hypothesis was partially confi rmed by fi nding that phosphatidyl-inositol-3-kinase, Akt kinase (Pl3K-Akt), and mitogen-activated MEK-Erk1/2 kinase inhibitors abolish the effect of apelin-13 on the mitochondrial pore opening and cardiomyocyte death [7,8,11]. Importantly that one of the targets of reperfusion kinases was endothelial NO synthase (eNOS), its expression increasing under the effect of apelin-13 [4,11]. Presumably, the protective effect of A-12 was also mediated by triggering of these mechanisms.…”

Section: Resultsmentioning

confidence: 97%

In Vivo Reduction of Reperfusion Injury to the Heart with Apelin-12 Peptide in Rats

et al. 2011

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Apelin-12 (A-12) peptide was synthesized by automated solid phase method and purified by reverse phase HPLC. Its homogeneity and structure were confirmed by HPLC, (1)H-NMR spectroscopy, and mass spectroscopy. Acute myocardial infarction was induced by 40-min occlusion of the left coronary artery with subsequent 60-min reperfusion in narcotized Wistar rats. Peptide A-12 was injected (intravenous bolus, 0.07 or 0.35 μmol/kg) to experimental animals simultaneously with the beginning of reperfusion. Injections of A-12 in these doses led to reduction of systolic BP to 67 and 85% of the initial level, respectively, which was virtually restored completely by the end of reperfusion, and to a significant reduction of the infarction focus in the myocardium (by 21 and 34% in comparison with the control, respectively). Injection of A-12 in a dose of 0.35 μmol/kg led to reduction of plasma concentrations of necrosis markers in comparison with the control by the end of reperfusion: MB-creatine kinase by 56%, lactate dehydrogenase by 30%. The results attest to vasodilatory effects of A-12 under conditions of heart reperfusion in vivo; the peptide injected after local ischemia limits the myocardial infarction size and reduces damage to cardiomyocyte membrane.

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“…AP stimulates NO production in the isolated rat aorta [37] and causes NOdependent arterial vasodilatation in vivo in humans [38]. Further, our previous experiments showed that at high doses AP had endothelium-dependent and partially NOindependent vasodilatory effects on Phe-precontracted rat pulmonary arteries [22].…”

Section: Discussionmentioning

confidence: 99%

Synergistic effects of apelin and leptin on isolated rat pulmonary arteries

et al. 2011

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AbstractApelin (AP) and leptin (LEP) are adipokines with vasomotor actions. Taking into account the published data on the role of obesity in the development of pulmonary hypertension, we studied the implications of apelin on leptin relaxing effects on isolated rat pulmonary arteries. LEP had vasodilatatory effects on phenylephrine-precontracted rat pulmonary arteries from normal and ovalbumin-sensitized rats, but not on rats with monocrotaline-induced pulmonary hypertension. AP13 pretreatment increased LEP effects by one-half. Our studies revealed the existence of synergistic favorable effects of these adipokines on pulmonary vessels.

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Apelin activates l-arginine/nitric oxide synthase/nitric oxide pathway in rat aortas

Cited by 104 publications

References 30 publications

Nitric oxide synthase mediates the apelin-induced improvement of myocardial postischemic metabolic and functional recovery

Nitric oxide synthase mediates the apelin-induced improvement of myocardial postischemic metabolic and functional recovery

In Vivo Reduction of Reperfusion Injury to the Heart with Apelin-12 Peptide in Rats

Synergistic effects of apelin and leptin on isolated rat pulmonary arteries

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