Nociceptin/orphanin FQ increases ANP secretion in neonatal cardiac myocytes

Kim, K.W.; Chung, Young Jin; Han, Jeong Hee; Woo, Ran-Sook; Park, E.Y.; Seul, Kyung Hwan; Kim, S.Z.; Cho, K.W.; Kim, S.H.

doi:10.1016/s0024-3205(01)01474-6

Cited by 14 publications

(5 citation statements)

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“…Opiods have been shown to increase ANP secretion in vivo and in isolated atria [62,63]. Crticotropin releasing factor also stimulates ANP secretion by what appears to be a direct receptor-mediated mechanism [64].…”

Section: Stimulation Of Anp Secretion By Other Neurohumoral Factorsmentioning

confidence: 99%

Mechanisms of atrial natriuretic peptide secretion from the atrium

Dietz

2005

Cardiovascular Research

158

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Since the discovery of atrial natriuretic peptide (ANP) more than 20 years ago, numerous studies have focused on the mechanisms regulating ANP secretion. From a physiological standpoint, the most important factor governing ANP secretion is mechanical stretching of the atria, which normally occurs when extracellular fluid volume or blood volume is elevated. In addition, the ability of several vasoconstrictors to increase ANP secretion can be traced to their indirect effects on atrial stretch via increases in cardiac preload or afterload. Whether vasoconstrictors such as angiotensin II and vasopressin have a direct positive or negative effect on ANP secretion has not been determined with certainty. Two paracrine factors derived from endothelial cells play important roles in modulating ANP secretion. Endothelin, a potent vasoconstrictor, stimulates ANP secretion and augments stretch induced ANP secretion. The dramatic increase in ANP release produced by cardiac ischemia appears to be mediated in part by endothelin. Nitric oxide (NO), an important vasodilator, is also produced by endothelial cells and inhibits ANP secretion acting through cyclic GMP as an intracellular messenger. Several recent studies have helped to define the cellular mechanism contributing to regulation of ANP secretion including stretch-activated ion channels, prostaglandins, cytochrome P450, G proteins and cell calcium. A number of steps in the cellular transduction of the ANP signal remain to be resolved. The release of ANP in disease states such as myocardial infarction and heart failure appears to be related to both mechanical and cellular events.

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Section: Stimulation Of Anp Secretion By Other Neurohumoral Factorsmentioning

confidence: 99%

Mechanisms of atrial natriuretic peptide secretion from the atrium

Dietz

2005

Cardiovascular Research

158

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“…Probably, δ-OR antagonists interact with high-affinity binding sites for des-Tyr-dalargin (e.g., ORL1 receptor or nonopiate dynorphin receptor). These receptors were found on cardiomyocyte membranes [10,11]. The ORL1 receptor is molecularly similar to κ-OR.…”

Section: Resultsmentioning

confidence: 96%

δ-opioid receptor antagonists exhibit properties of partial δ-receptor agonists in isolated perfused heart

Maslov¹,

Ласукова²,

Bespalova³

et al. 2004

Bull Exp Biol Med

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Perfusion of the isolated intact rat heart with Krebs-Henseleit solution containing agonists ((-)-TAN-67, DPDPE, and dalargin) or antagonists of delta-opioid receptors (naltrindole, TIPP[psi], and ICI 174,864) in a final concentration of 0.1 mg/liter was followed by a decrease in the heart rate, end-diastolic pressure, contraction rate, relaxation rate, and left ventricular developed pressure. Perfusion with a solution containing the delta-opioid receptor agonist DPDPE or delta-antagonists naltrindole, TIPP[psi], and ICI 174,864 before modeling of global ischemia increased the severity of reperfusion-induced contractile dysfunction in the myocardium. Our results suggest that delta-opioid receptor antagonists in vitro exhibit properties of partial delta-receptor agonists.

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“…Affinity for opioid-like receptors is due to the peptide fragment Phe-X-Gly-Phe [25], which is present in the structures of both NALE and G peptides. Opioid-like receptors are present on the CMC membrane [26] and are likely to be involved in the cardiotropic properties of NALE and G peptide.…”

Section: Discussionmentioning

confidence: 99%

The Role Of Amino Acid Arginine And Nitric Oxide System In Implementing Cardioprotective Effect Of Non-Opioid Analogue Of Leu-Enkephalin In Newborn Albino Rats After Intrauterine Hypoxia

et al. 2020

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Objective ― to evaluate the role of the amino acid arginine in the structure of the non-opioid analogue of leu-enkephalin (NALE) and the involvement of the nitric oxide system in the implementation of its cardioprotective effect in newborn albino rats subjected to intrauterine hypoxia. Material and Methods ― Pregnant female rats were subjected daily to 4-hour hypobaric hypoxia (oxygen partial pressure – 65 mm Hg) on days 15-19 of their gestation. The 7-day-old offspring of hypoxified female rats were examined. The progeny of intact animals served the control. We studied body and heart weights; activity of proliferative processes and autophagy in the myocardium of subendocardial parts of the left ventricle, expressed via the immunohistochemical detection of Ki-67 and Beclin-1 proteins, respectively; karyometric and nucleolometric indicators of cardiomyocytes (CMC); intensity of free radical processes in the tissues of the heart by chemiluminescence parameters. Correction of post-hypoxic changes in newborn rats was carried out by intraperitoneal injection of two peptides (Phe–D-Ala–Gly–Phe–Leu–Arg – non-opioid analogue of leu-enkephalin, or NALE, and Phe–D-Ala–Gly–Phe–Leu–Gly – G peptide) daily from day 2 through day 6 of their lives at a dose of 100 μg/kg. To assess the involvement of the nitric oxide system in the implementation of the NALE effects, the NO synthase inhibitor – N-nitro-L-arginine methyl ester (L-NAME) was additionally administered at a dose of 50 mg/kg. Results ― Intrauterine hypoxia led to a decrease in body weights of 7-day-old animals, an increase in the number of CMC expressing the Beclin-1 protein, reduction in the size of CMC nuclei, activation of free radial oxidation, and a decrease in antiradical protection in the heart tissues. The administration of NALE to newborn animals, subjected to intrauterine hypoxia (IUH), normalized their body weight and size of the CMC nuclei, and partially corrected changes in Beclin-1 expression and in chemiluminescence parameters. In 7-day-old animals, subjected to IUH and neonatal administration of NALE and L-NAME, a lower body weight was observed than in the control. Against the background of nitric oxide blockade, the antioxidant effect of NALE diminished, but the corrective effect of NALE on the karyometric index and Beclin-1 expression remained. G peptide, which differs from NALE by the substitution of the C-terminal amino acid Arg for the amino acid Gly, exhibited a corrective effect similar to NALE on the consequences of IUH. Conclusion ― Administration of NALE and G peptides to newborn albino rats after IUH has a pronounced cardioprotective effect. The mechanisms of the NALE peptide effects are, in part, associated with the activation of the NOS-NO system. However, the affinity of this peptide for opioid-like receptors may be of greater importance.

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Nociceptin/orphanin FQ increases ANP secretion in neonatal cardiac myocytes

Cited by 14 publications

References 0 publications

Mechanisms of atrial natriuretic peptide secretion from the atrium

Mechanisms of atrial natriuretic peptide secretion from the atrium

δ-opioid receptor antagonists exhibit properties of partial δ-receptor agonists in isolated perfused heart

The Role Of Amino Acid Arginine And Nitric Oxide System In Implementing Cardioprotective Effect Of Non-Opioid Analogue Of Leu-Enkephalin In Newborn Albino Rats After Intrauterine Hypoxia

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