ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2013
Regulation of renin release via cyclic ADP-ribose-mediated signaling: evidence from mice lacking CD38 gene.
Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Genome-Wide Meta-Analysis of Blood Pressure Response to βJournal of the American Heart Association · 2019Pooled it
- Possible Molecular Mechanisms of Hypertension Induced by Sleep Apnea Syndrome/Intermittent Hypoxia.Life (Basel, Switzerland) · 2024Review
- The Impact of Intermittent Hypoxia on Metabolism and Cognition.International journal of molecular sciences · 2022Review
- Intermittent Hypoxia Upregulates theInternational journal of molecular sciences · 2021Article
- Some Aspects of the Renin-Angiotensin-System in Hemodialysis Patients.Kidney & blood pressure research · 2015Review
- Roles of NAD (+) , PARP-1, and Sirtuins in Cell Death, Ischemic Brain Injury, and Synchrotron Radiation X-Ray-Induced Tissue Injury.Scientifica · 2013Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND/
aimsDespite extensive studies, the intracellular regulatory mechanism of renin production and release is still poorly understood. The present study was designed to test whether CD38-ADP-ribosylcyclase signaling pathway contributes to the regulation of renin production and release, and to examine whether CD38 gene knockout (CD38(-/-)) can change this important renal endocrinal function.
methodsADP-ribosylcyclase activity was estimated utilizing HPLC, cADPR levels from western blot, plasma renin activity from RIA kit, urinary sodium and potassium excretion from fame photometry.
resultsThe expression of CD38 and the activity of ADP-ribosylcyclase to produce cyclic ADP-ribose (cADPR) were nearly abolished in the kidney from CD38(-/-) mice, indicating that CD38 gene is a major enzyme responsible for the generation of cADPR in vivo. Mice lacking CD38 gene showed increased plasma renin activity (PRA) in either conscious or anesthetized status (P<0.05). Low salt intake significantly increased, but high salt intake significantly decreased renin release in both CD38(+/+) and CD38(-/-) mice. In acute experiments, it was demonstrated that plasma renin activity (PRA) significantly increased upon isoprenaline infusion in CD38(-/-) mice compared to CD38(+/+) mice. Accompanied with such increase in PRA, glomerular filtration rate (GFR), renal blood flow (RBF), urine volume (UV) and sodium excretion (UNaV) more significantly decreased in CD38(-/-) than CD38(+/+) mice. Similarly, more increases in PRA but more decreases in GFR, RBF, UV and UNaV were observed in CD38(-/-) than CD38(+/+) mice when they had a low renal perfusion pressure (RPP).
conclusionCD38-cADPR-mediated signaling may importantly contribute to the maintenance of low PRA and participate in the regulation of renal hemodynamics and excretory function in mice.
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