ArticleThe Journal of clinical investigation1995
Vasopressin resistance in chronic renal failure. Evidence for the role of decreased V2 receptor mRNA.
Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 76 citations in OpenAlex.
- Abnormal urinary excretion of NKCC2 and AQP2 in response to hypertonic saline in chronic kidney disease: an intervention study in patients with chronic kidney disease and healthy controls.BMC nephrology · 2014Trial
- Copeptin levels associate with cardiovascular events in patients with ESRD and type 2 diabetes mellitus.Journal of the American Society of Nephrology : JASN · 2011Trial
- Association between kidney function and risk of hyponatremia: a single-center, cross-sectional study in the outpatient setting.Clinical and experimental nephrology · 2026Article
- Article
- The urine-to-plasma urea concentration ratio is associated with eGFR and eGFR decline over time in a population cohort.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023Article
- Dysnatremias in Chronic Kidney Disease: Pathophysiology, Manifestations, and Treatment.Frontiers in medicine · 2021Review
- Impact of serum albumin levels on the body fluid response to tolvaptan in chronic kidney disease patients.International urology and nephrology · 2019Article
- Vasopressin-aquaporin-2 pathway: recent advances in understanding water balance disorders.F1000Research · 2019Review
- Hereditary Nephrogenic Diabetes Insipidus: Pathophysiology and Possible Treatment. An Update.International journal of molecular sciences · 2017Review
- High Water Intake and Progression of Chronic Kidney Diseases.Electrolyte & blood pressure : E & BP · 2015Review
- Management of severe hyponatremia: infusion of hypertonic saline and desmopressin or infusion of vasopressin inhibitors?The American journal of the medical sciences · 2014Review
- Dysnatremias in patients with kidney disease.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2014Review
- Nephrogenic diabetes insipidus: essential insights into the molecular background and potential therapies for treatment.Endocrine reviews · 2013Review
- Physiology and pathophysiology of the vasopressin-regulated renal water reabsorption.Pflugers Archiv : European journal of physiology · 2008Review
- Angiotensin II AT1 receptor blockade changes expression of renal sodium transporters in rats with chronic renal failure.Journal of Korean medical science · 2005Article
- Severe Burn Injuries - The Day the Sodium Starts Rising.In vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Studies were performed to determine the mechanism underlying deficient arginine vasopressin (AVP)-stimulated adenylyl cyclase activity in chronic renal failure (CRF). As compared to control, principal cells cultured from the inner medullary collecting tubule of rats previously made uremic by 5/6 nephrectomy fail to accumulate cAMP when stimulated with AVP. CRF cells do respond normally to forskolin or cholera toxin and the defect in AVP responsiveness is not prevented by treatment with pertussis toxin, by cyclooxygenase inhibition, or by inhibition or down-regulation of protein kinase C. In contrast to their lack of responsiveness to AVP, CRF cells respond normally to other agonists of adenylyl cyclase such as isoproterenol or prostaglandin E2. Plasma membranes prepared from the inner medullae of CRF rats exhibit a marked decrease in apparent AVP receptor number but no change in the apparent number of beta adrenergic receptors. Reverse transcriptase PCR of total RNA from the inner medullae of CRF animals reveals virtual absence of V2 receptor mRNA; mRNA for alpha s is present in normal abundance. These studies indicate that AVP resistance in CRF is due, at least in part, to selective down-regulation of the V2 receptor as a consequence of decreased V2 receptor mRNA.
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What OpenQuestion holds
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.