ArticleAmerican journal of physiology. Renal physiology2012
Renal afferent arteriolar and tubuloglomerular feedback reactivity in mice with conditional deletions of adenosine 1 receptors.
Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- G protein-coupled receptor-mediated renal fibrosis: a key focus on kidney disease drug development.Frontiers in pharmacology · 2025Review
- Adenosine signaling as target in cardiovascular pharmacology.Current opinion in pharmacology · 2023Review
- Maladaptation of renal hemodynamics contributes to kidney dysfunction resulting from thoracic spinal cord injury in mice.American journal of physiology. Renal physiology · 2022Article
- Update on Pathogenesis of Glomerular Hyperfiltration in Early Diabetic Kidney Disease.Frontiers in endocrinology · 2022Review
- Adenosine Receptor Reserve and Long-Term Potentiation: Unconventional Adaptive Mechanisms in Cardiovascular Diseases?International journal of molecular sciences · 2021Review
- Purinoceptors, renal microvascular function and hypertension.Physiological research · 2020Review
- Adenosine and the Cardiovascular System: The Good and the Bad.Journal of clinical medicine · 2020Review
- Adenosine Receptors Influence Hypertension in Dahl Salt-Sensitive Rats: Dependence on Receptor Subtype, Salt Diet, and Sex.Hypertension (Dallas, Tex. : 1979) · 2018Article
- CD39-adenosinergic axis in renal pathophysiology and therapeutics.Purinergic signalling · 2018Review
- The effects of dual PPARPhysiological reports · 2017Article
- Renal autoregulation in health and disease.Physiological reviews · 2015Review
- Purinergic signalling in the kidney in health and disease.Purinergic signalling · 2014Review
- A prospective assessment of the effect of aminophylline therapy on urine output and inflammation in critically ill children.Frontiers in pediatrics · 2014Article
- Role of CD73 in Renal Sympathetic Neurotransmission in the Mouse Kidney.Physiological reports · 2013Article
- Direct assessment of tubuloglomerular feedback responsiveness in connexin 40-deficient mice.American journal of physiology. Renal physiology · 2013Article
- Tubuloglomerular feedback and renal function in mice with targeted deletion of the type 1 equilibrative nucleoside transporter.American journal of physiology. Renal physiology · 2013Article
- Aminophylline for improving acute kidney injury in pediatric patients: A systematic review and meta-analysis.International journal of health sciencesReview
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Adenosine 1 receptors (A1AR) have been shown in previous experiments to play a major role in the tubuloglomerular feedback (TGF) constrictor response of afferent arterioles (AA) to increased loop of Henle flow. Overexpression studies have pointed to a critical role of vascular A1AR, but it has remained unclear whether selective deletion of A1AR from smooth muscle cells is sufficient to abolish TGF responsiveness. To address this question, we have determined TGF response magnitude in mice in which vascular A1AR deletion was achieved using the loxP recombination approach with cre recombinase being controlled by a smooth muscle actin promoter (SmCre/A1ARff). Effective vascular deletion of A1AR was affirmed by absence of vasoconstrictor responses to adenosine or cyclohexyl adenosine (CHA) in microperfused AA. Elevation of loop of Henle flow from 0 to 30 nl/min caused a 22.1 ± 3.1% reduction of stop flow pressure in control mice and of 7.2 ± 1.5% in SmCre/A1ARff mice (P < 0.001). Maintenance of residual TGF activity despite absence of A1AR-mediated responses in AA suggests participation of extravascular A1AR in TGF. Support for this notion comes from the observation that deletion of A1ARff by nestin-driven cre causes an identical TGF response reduction (7.3 ± 2.4% in NestinCre/A1ARff vs. 20.3 ± 2.7% in controls), whereas AA responsiveness was reduced but not abolished. A1AR on AA smooth muscle cells are primarily responsible for TGF activation, but A1AR on extravascular cells, perhaps mesangial cells, appear to contribute to the TGF response.
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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.