Inhibition of endogenous ouabain by atrial natriuretic peptide is a guanylyl cyclase independent effect

<h4>Background</h4> Endogenous ouabain (EO) and atrial natriuretic peptide (ANP) are important in regulation of sodium and fluid balance. There is indirect evidence that ANP may be involved in the regulation of endogenous cardenolides. <h4>Methods</h4> H295R are human adrenoc...

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Autores principales:	Gulay Tegin, Yonglin Gao, John M. Hamlyn, Barbara J. Clark, Rif S. El-Mallakh
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/018131678c4d49269d480a0d25e6321e
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spelling	oai:doaj.org-article:018131678c4d49269d480a0d25e6321e2021-11-25T06:19:44ZInhibition of endogenous ouabain by atrial natriuretic peptide is a guanylyl cyclase independent effect1932-6203https://doaj.org/article/018131678c4d49269d480a0d25e6321e2021-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8601428/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4> Endogenous ouabain (EO) and atrial natriuretic peptide (ANP) are important in regulation of sodium and fluid balance. There is indirect evidence that ANP may be involved in the regulation of endogenous cardenolides. <h4>Methods</h4> H295R are human adrenocortical cells known to release EO. Cells were treated with ANP at physiologic concentrations or vehicle (0.1% DMSO), with or without guanylyl cyclase inhibitor 1,2,4 oxadiazolo[4,3-a]quinoxalin-1-one (ODQ). Cyclic guanosine monophosphate (cGMP), the intracellular second messenger of ANP, was measured by a chemiluminescent immunoassay and EO was measured by radioimmunoassay of C18 extracted samples. <h4>Results</h4> EO secretion is inhibited by ANP treatment, with the most prolonged inhibition (90 min vs ≤ 60 min) occurring at physiologic ANP concentrations (50 pg/mL). Inhibition of guanylyl cyclase with ODQ, also reduces EO secretion. The inhibitory effects on EO release in response to cotreatment with ANP and ODQ appeared to be additive. <h4>Conclusions</h4> ANP inhibits basal EO secretion, and it is unlikely that this is mediated through ANP-A or ANP-B receptors (the most common natriuretic peptide receptors) or their cGMP second messenger; the underlying mechanisms involved are not revealed in the current studies. The role of ANP in the control of EO synthesis and secretion in vivo requires further investigation.Gulay TeginYonglin GaoJohn M. HamlynBarbara J. ClarkRif S. El-MallakhPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Gulay Tegin Yonglin Gao John M. Hamlyn Barbara J. Clark Rif S. El-Mallakh Inhibition of endogenous ouabain by atrial natriuretic peptide is a guanylyl cyclase independent effect
description	<h4>Background</h4> Endogenous ouabain (EO) and atrial natriuretic peptide (ANP) are important in regulation of sodium and fluid balance. There is indirect evidence that ANP may be involved in the regulation of endogenous cardenolides. <h4>Methods</h4> H295R are human adrenocortical cells known to release EO. Cells were treated with ANP at physiologic concentrations or vehicle (0.1% DMSO), with or without guanylyl cyclase inhibitor 1,2,4 oxadiazolo[4,3-a]quinoxalin-1-one (ODQ). Cyclic guanosine monophosphate (cGMP), the intracellular second messenger of ANP, was measured by a chemiluminescent immunoassay and EO was measured by radioimmunoassay of C18 extracted samples. <h4>Results</h4> EO secretion is inhibited by ANP treatment, with the most prolonged inhibition (90 min vs ≤ 60 min) occurring at physiologic ANP concentrations (50 pg/mL). Inhibition of guanylyl cyclase with ODQ, also reduces EO secretion. The inhibitory effects on EO release in response to cotreatment with ANP and ODQ appeared to be additive. <h4>Conclusions</h4> ANP inhibits basal EO secretion, and it is unlikely that this is mediated through ANP-A or ANP-B receptors (the most common natriuretic peptide receptors) or their cGMP second messenger; the underlying mechanisms involved are not revealed in the current studies. The role of ANP in the control of EO synthesis and secretion in vivo requires further investigation.
format	article
author	Gulay Tegin Yonglin Gao John M. Hamlyn Barbara J. Clark Rif S. El-Mallakh
author_facet	Gulay Tegin Yonglin Gao John M. Hamlyn Barbara J. Clark Rif S. El-Mallakh
author_sort	Gulay Tegin
title	Inhibition of endogenous ouabain by atrial natriuretic peptide is a guanylyl cyclase independent effect
title_short	Inhibition of endogenous ouabain by atrial natriuretic peptide is a guanylyl cyclase independent effect
title_full	Inhibition of endogenous ouabain by atrial natriuretic peptide is a guanylyl cyclase independent effect
title_fullStr	Inhibition of endogenous ouabain by atrial natriuretic peptide is a guanylyl cyclase independent effect
title_full_unstemmed	Inhibition of endogenous ouabain by atrial natriuretic peptide is a guanylyl cyclase independent effect
title_sort	inhibition of endogenous ouabain by atrial natriuretic peptide is a guanylyl cyclase independent effect
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/018131678c4d49269d480a0d25e6321e
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Inhibition of endogenous ouabain by atrial natriuretic peptide is a guanylyl cyclase independent effect

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