2022
DOI: 10.3389/fphys.2021.787598
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A Vasopressin-Induced Change in Prostaglandin Receptor Subtype Expression Explains the Differential Effect of PGE2 on AQP2 Expression

Abstract: Arginine vasopressin (AVP) stimulates the concentration of renal urine by increasing the principal cell expression of aquaporin-2 (AQP2) water channels. Prostaglandin E2 (PGE2) and prostaglandin2α (PGF2α) increase the water absorption of the principal cell without AVP, but PGE2 decreases it in the presence of AVP. The underlying mechanism of this paradoxical response was investigated here. Mouse cortical collecting duct (mkpCCDc14) cells mimic principal cells as they endogenously express AQP2 in response to AV… Show more

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Cited by 4 publications
(3 citation statements)
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“…8 However, inhibition of these hemodynamic responses to furosemide administration was considered unlikely to contribute substantially to attenuation of furosemide-induced diuresis. 4,27 Currently, this complex interaction of PGE 2 with its multiple receptors is incompletely understood but in studies examining the effects of NSAIDs on furosemide-induced diuresis, NSAIDs attenuate diuresis by up to 50%. 3,4,6 Our study was not designed to determine the mechanism(s) by which NSAIDs attenuate furosemide-induced diuresis; thus, the pro-…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…8 However, inhibition of these hemodynamic responses to furosemide administration was considered unlikely to contribute substantially to attenuation of furosemide-induced diuresis. 4,27 Currently, this complex interaction of PGE 2 with its multiple receptors is incompletely understood but in studies examining the effects of NSAIDs on furosemide-induced diuresis, NSAIDs attenuate diuresis by up to 50%. 3,4,6 Our study was not designed to determine the mechanism(s) by which NSAIDs attenuate furosemide-induced diuresis; thus, the pro-…”
Section: Discussionmentioning
confidence: 99%
“…PGE 2 action on EP4 and EP2 receptors increase intracellular cAMP, promoting phosphorylation, translocation, and expression of aquaporin 2 (AQP2), thereby increasing collecting duct water permeability and urine concentration. In contrast, PGE 2 action on EP1 and EP3 receptors appears to downregulate AQP2 function by increasing intracellular Ca ++ and attenuating cAMP production, respectively, leading to diuresis 4,27 . Currently, this complex interaction of PGE 2 with its multiple receptors is incompletely understood but in studies examining the effects of NSAIDs on furosemide‐induced diuresis, NSAIDs attenuate diuresis by up to 50% 3,4,6 …”
Section: Discussionmentioning
confidence: 99%
“…2 PGE2 can either increase or decrease water reabsorption depending on the E-prostanoid (EP) receptor subtypes that are expressed and whether vasopressin is present or absent. 3,4 PGE2 is rapidly metabolized in the kidney to inactive PGE2 metabolite (PGEM) and excreted in urine as both PGE2 and PGEM. 5 Patients with autosomal dominant polycystic kidney disease (ADPKD) develop a urinary concentrating defect early in the course of the disease.…”
Section: Introductionmentioning
confidence: 99%