ArticleProceedings of the National Academy of Sciences of the United States of America1999
Atrial natriuretic peptide and oxytocin induce natriuresis by release of cGMP.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 110 citations in OpenAlex.
- Knockdown of the type 1 cannabinoid receptor in the central amygdala increases both spontaneous and water deprivation-induced sodium intake in rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Oxytocin in Women's Health and Disease.Frontiers in endocrinology · 2022Review
- Cardiovascular Neuroendocrinology: Emerging Role for Neurohypophyseal Hormones in Pathophysiology.Endocrinology · 2021Review
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- Effects of endogenous HMolecular and cellular biochemistry · 2021Article
- Sex Differences in the Regulation of Vasopressin and Oxytocin Secretion in Bile Duct-Ligated Rats.Neuroendocrinology · 2021Article
- Vasopressin and oxytocin expression in hypothalamic supraoptic nucleus and plasma electrolytes changes in water-deprived maleAnimal cells and systems · 2021Article
- The Role of Oxytocin in Cardiovascular Protection.Frontiers in psychology · 2020Review
- Therapeutic Potential of Oxytocin in Atherosclerotic Cardiovascular Disease: Mechanisms and Signaling Pathways.Frontiers in neuroscience · 2019Review
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- Increased Activity of the Intracardiac Oxytocinergic System in the Development of Postinfarction Heart Failure.BioMed research international · 2016Article
- The role of oxytocin in cardiovascular regulation.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014Review
- Article
- Annexin A1 complex mediates oxytocin vesicle transport.Journal of neuroendocrinology · 2013Article
- Oxytocin: an unexpected risk for cardiologic and broncho-obstructive effects, and allergic reactions in susceptible delivering women.Multidisciplinary respiratory medicine · 2013Article
- Oxytocin: Old Hormone, New Drug.Pharmaceuticals (Basel, Switzerland) · 2009Review
- Article
- Resting and circadian release of nitric oxide is controlled by leptin in male rats.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Oxytocin and its receptors are synthesized in the rat vasculature.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Corticotropin-releasing hormone causes antidiuresis and antinatriuresis by stimulating vasopressin and inhibiting atrial natriuretic peptide release in male rats.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Our hypothesis is that oxytocin (OT) causes natriuresis by activation of renal NO synthase that releases NO followed by cGMP that mediates the natriuresis. To test this hypothesis, an inhibitor of NO synthase, L-nitroarginine methyl ester (NAME), was injected into male rats. Blockade of NO release by NAME had no effect on natriuresis induced by atrial natriuretic peptide (ANP). This natriuresis presumably is caused by cGMP because ANP also activates guanylyl cyclase, which synthesizes cGMP from GTP. The 18-fold increase in sodium (Na+) excretion induced by OT (1 microgram) was accompanied by an increase in urinary cGMP and preceded by 20 min a 20-fold increase in NO3- excretion. NAME almost completely inhibited OT-induced natriuresis and increased NO3- excretion; however, when the dose of OT was increased 10-fold, a dose that markedly increases plasma ANP concentrations, NAME only partly inhibited the natriuresis. We conclude that the natriuretic action of OT is caused by a dual action: generation of NO leading to increased cGMP and at higher doses release of ANP that also releases cGMP. OT-induced natriuresis is caused mainly by decreased tubular Na+ reabsorption mediated by cGMP. In contrast to ANP that releases cGMP in the renal vessels and the tubules, OT acts on its receptors on NOergic cells demonstrated in the macula densa and proximal tubules to release cGMP that closes Na+ channels. Both ANP- and OT-induced kaliuresis also appear to be mediated by cGMP. We conclude that cGMP mediates natriuresis and kaliuresis induced by both ANP and OT.
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