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

Autor: Barbara J. Clark, John M. Hamlyn, Gulay Tegin, Rif S. El-Mallakh, Yonglin Gao
Rok vydání: 2021
Předmět:
Physiology
Vasodilator Agents
Peptide Hormones
Endogeny
Blood Pressure
Pharmacology
Second Messenger Systems
Biochemistry
Vascular Medicine
chemistry.chemical_compound
Atrial natriuretic peptide
Natriuretic peptide
Medicine and Health Sciences
Lipid Hormones
Receptor
Ouabain
Cyclic GMP
Aldosterone
Oxadiazoles
Multidisciplinary
Organic Compounds
Chemistry
Second messenger system
Physical Sciences
cardiovascular system
Medicine
Steroids
Biological Cultures
hormones
hormone substitutes
and hormone antagonists

Atrial Natriuretic Factor
circulatory and respiratory physiology
Research Article
medicine.drug_class
Science
Radioimmunoassay
Receptors
Cell Surface

Research and Analysis Methods
Radioimmunoassays
Natriuretic Peptide
Cell Line
Tumor

Quinoxalines
medicine
Humans
Secretion
Immunoassays
Cyclic guanosine monophosphate
Organic Chemistry
Chemical Compounds
Biology and Life Sciences
Cell Cultures
Peptide Fragments
Hormones
Atrial Natriuretic Peptide
chemistry
Guanylate Cyclase
Adrenal Cortex
Immunologic Techniques
Physiological Processes
Receptors
Atrial Natriuretic Factor
Zdroj: PLoS ONE
PLoS ONE, Vol 16, Iss 11 (2021)
PLoS ONE, Vol 16, Iss 11, p e0260131 (2021)
ISSN: 1932-6203
Popis: Background 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. Methods 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. Results 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. Conclusions 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.
Databáze: OpenAIRE