ArticleHypertension (Dallas, Tex. : 1979)2009
Possible mediators of connecting tubule glomerular feedback.
Article in Hypertension (Dallas, Tex. : 1979), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 34 citations in OpenAlex.
- Luminal Flow in the Connecting Tubule induces Afferent Arteriole Vasodilation.bioRxiv : the preprint server for biology · 2024Article
- Epithelial N-methyl-D-aspartate (NMDA) receptors mediate renal vasodilation by affecting kidney autoregulation.bioRxiv : the preprint server for biology · 2023Article
- G protein-coupled estrogen receptor: a promising therapeutic target for aldosterone-induced hypertension.Frontiers in endocrinology · 2023Review
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- Kidney Microcirculation as a Target for Innovative Therapies in AKI.Journal of clinical medicine · 2021Review
- Sensing of tubular flow and renal electrolyte transport.Nature reviews. Nephrology · 2020Review
- Tubule-vascular feedback in renal autoregulation.American journal of physiology. Renal physiology · 2019Review
- A Novel Mechanism of Renal Microcirculation Regulation: Connecting Tubule-Glomerular Feedback.Current hypertension reports · 2019Review
- Role of connecting tubule glomerular feedback in obesity related renal damage.American journal of physiology. Renal physiology · 2018Article
- Connecting tubule glomerular feedback mediates tubuloglomerular feedback resetting after unilateral nephrectomy.American journal of physiology. Renal physiology · 2018Article
- Mechanisms of connecting tubule glomerular feedback enhancement by aldosterone.American journal of physiology. Renal physiology · 2016Article
- Effects of renal Na+/Ca2+ exchanger 1 inhibitor (SEA0400) treatment on electrolytes, renal function and hemodynamics in rats.Clinical and experimental nephrology · 2015Article
- Renal autoregulation in health and disease.Physiological reviews · 2015Review
- Aldosterone sensitizes connecting tubule glomerular feedback via the aldosterone receptor GPR30.American journal of physiology. Renal physiology · 2014Article
- ATP acting through P2Y receptors causes activation of podocyte TRPC6 channels: role of podocin and reactive oxygen species.American journal of physiology. Renal physiology · 2014Article
- P2 receptors in renal autoregulation.Current vascular pharmacology · 2014Review
- Prostaglandin E2 mediates connecting tubule glomerular feedback.Hypertension (Dallas, Tex. : 1979) · 2013Article
- Chronic kidney disease: Mesoamerican nephropathy--new clues to the cause.Nature reviews. Nephrology · 2013Article
- Connecting tubule glomerular feedback in hypertension.Hypertension (Dallas, Tex. : 1979) · 2013Article
- Central systolic augmentation indexes and urinary sodium in a white population.American journal of hypertension · 2013Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
In the renal cortex, the connecting tubule (CNT) returns to the glomerular hilum and contacts the afferent arteriole (Af-Art). Increasing Na delivery to the CNT dilates the Af-Art by activating epithelial Na channels, a process that we call connecting tubule glomerular feedback (CTGF). However, the mediator(s) of CTGF are unknown. We tested the hypothesis that Na reabsorption by the CNT induces release of arachidonic acid metabolites that diffuse to and dilate the Af-Art. Microdissected rabbit Af-Arts and adherent CNTs were simultaneously microperfused. CTGF was measured as the increase in diameter of norepinephrine-preconstricted Af-Arts in response to switching NaCl concentration in the lumen of the CNT from 10 to 80 mmol/L. Under control conditions, CTGF was repeatable and completely reversed norepinephrine-induced vasoconstriction. In the presence of 5,8,11,14-eicosatetraynoic acid, an inhibitor of arachidonic acid metabolism, CTGF was completely blocked (-0.7+/-0.3 versus 7.3+/-0.5 microm), suggesting that arachidonic acid metabolites mediate CTGF. Because both cyclooxygenase-derived prostaglandins and epoxygenase-derived epoxyeicosatrienoic acids are known vasodilatory arachidonic acid metabolites, we tested whether indomethacin or MS-PPOH (a cyclooxygenase and an epoxygenase inhibitor) could block CTGF. Both indomethacin and MS-PPOH partially blocked CTGF (2.3+/-0.8 versus 6.5+/-0.5 microm, and 2.9+/-0.8 versus 6.6+/-1.1 microm, respectively). When combined, they completely blocked CTGF (-0.4+/-0.3 versus 6.6+/-1.1 microm). We confirmed these findings by using the epoxyeicosatrienoic acid antagonist 14,15-EEZE. The combination of indomethacin plus 14,15-EEZE completely abolished CTGF (-0.3+/-0.2 versus 8.0+/-1.0 microm). We conclude that increasing Na concentrations in the CNT stimulate release of prostaglandins and epoxyeicosatrienoic acids, which mediate CTGF.
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