ArticleProceedings of the National Academy of Sciences of the United States of America1998
Stimulation of renin secretion by nitric oxide is mediated by phosphodiesterase 3.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03307655 (Relationship Between Nitric Oxide), which is not on this map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Relationship Between Nitric Oxide (NO) in Follicular Fluid and Sperm Fertilization Ability
Who cites it
23 citing papers in PubMed, 101 citations in OpenAlex.
- Crosstalk between renin and arachidonic acid (and its metabolites).Lipids in health and disease · 2025Review
- Editorial: Cyclic nucleotide phosphodiesterases (PDEs) signaling in the endocrine system.Frontiers in endocrinology · 2025Article
- Regulation of the renin-angiotensin-aldosterone system by cyclic nucleotides and phosphodiesterases.Frontiers in endocrinology · 2023Review
- Review
- Low Nitric Oxide Bioavailability Increases Renin Production in the Collecting Duct.Frontiers in physiology · 2020Article
- Protein Kinase G Is Involved in Acute but Not in Long-Term Regulation of Renin Secretion.Frontiers in pharmacology · 2019Article
- Analysis of the calcium paradox of renin secretion.American journal of physiology. Renal physiology · 2018Article
- Role of Phosphodiesterase 5 and Cyclic GMP in Hypertension.Current hypertension reports · 2016Review
- Classical Renin-Angiotensin system in kidney physiology.Comprehensive Physiology · 2014Review
- Endothelium-derived nitric oxide supports renin cell recruitment through the nitric oxide-sensitive guanylate cyclase pathway.Hypertension (Dallas, Tex. : 1979) · 2013Article
- The influence of extracellular and intracellular calcium on the secretion of renin.Pflugers Archiv : European journal of physiology · 2013Review
- Tubular control of renin synthesis and secretion.Pflugers Archiv : European journal of physiology · 2013Review
- Regulation of renin secretion by renal juxtaglomerular cells.Pflugers Archiv : European journal of physiology · 2013Review
- Convergence of major physiological stimuli for renin release on the Gs-alpha/cyclic adenosine monophosphate signaling pathway.Clinical and experimental nephrology · 2012Review
- Stimulation of renin secretion by angiotensin II blockade is Gsalpha-dependent.Journal of the American Society of Nephrology : JASN · 2010Article
- The role of calcium in the regulation of renin secretion.American journal of physiology. Renal physiology · 2010Review
- Simultaneous changes of cell volume and cytosolic calcium concentration in macula densa cells caused by alterations of luminal NaCl concentration.The Journal of physiology · 2005Article
- Cyclic nucleotide phosphodiesterases in pancreatic islets.Diabetologia · 2003Review
- Promoter activity of the 5'-flanking regions of medaka fish soluble guanylate cyclase alpha1 and beta1 subunit genes.The Biochemical journal · 2002Article
- LXRalpha functions as a cAMP-responsive transcriptional regulator of gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to characterize the cellular pathways along which nitric oxide (NO) stimulates renin secretion from the kidney. Using the isolated perfused rat kidney model we found that renin secretion stimulated 4- to 8-fold by low perfusion pressure (40 mmHg), by macula densa inhibition (100 micromol/liter of bumetanide), and by adenylate cyclase activation (3 nmol/liter of isoproterenol) was markedly attenuated by the NO synthase inhibitor nitro-L-arginine methyl ester (L-Name) (1 mM) and that the inhibition by L-Name was compensated by the NO-donor sodium nitroprusside (SNP) (10 micromol/liter). Similarly, inhibition of cAMP degradation by blockade of phosphodiesterase 1 (PDE-1) (20 micromol/liter of 8-methoxymethyl-1-methyl-3-(2-methylpropyl)xanthine) or of PDE-4 (20 micromol/liter of rolipram) caused a 3- to 4-fold stimulation of renin secretion that was attenuated by L-Name and that was even overcompensated by sodium nitroprusside. Inhibition of PDE-3 by 20 micromol/liter of milrinone or by 200 nmol/liter of trequinsin caused a 5- to 6-fold stimulation of renin secretion that was slightly enhanced by NO synthase inhibition and moderately attenuated by NO donation. Because PDE-3 is a cGMP-inhibited cAMP-PDE the role of endogenous cGMP for the effects of NO was examined by the use of the specific guanylate cyclase inhibitor 1-H-(1,2,4)oxodiazolo(4,3a)quinoxalin-1-one (20 micromol). In the presence of 1H-[1,2,4]oxodiazolo[4,3-a]quinoxalin-1-one the effect of NO on renin secretion was abolished, whereas PDE-3 inhibitors exerted their normal effects. These findings suggest that PDE-3 plays a major role for the cAMP control of renin secretion. Our findings are compatible with the idea that the stimulatory effects of endogenous and exogenous NO on renin secretion are mediated by a cGMP-induced inhibition of cAMP degradation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.