scholarly journals Apelin Counteracts Vasopressin-Induced Water Reabsorption via Cross Talk Between Apelin and Vasopressin Receptor Signaling Pathways in the Rat Collecting Duct

Endocrinology ◽  
2014 ◽  
Vol 155 (11) ◽  
pp. 4483-4493 ◽  
Author(s):  
Annette Hus-Citharel ◽  
Laurence Bodineau ◽  
Alain Frugière ◽  
Fanny Joubert ◽  
Nadine Bouby ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Cross Talk ◽  
Arginine Vasopressin ◽  
Blood Circulation ◽  
Direct Action ◽  
Collecting Duct ◽  
Urine Osmolality ◽  
Water Reabsorption ◽  
Collecting Ducts ◽  
Antagonist Effect

Abstract Apelin receptors (ApelinRs) are expressed along an increasing cortico-medullary gradient in collecting ducts (CDs). We showed here that iv injection of apelin 17 (K17F) in lactating rats characterized by increases in both synthesis and release of arginine vasopressin (AVP) increased diuresis concomitantly with a significant decrease in urine osmolality and no change in Na+ and K+ excretion. Under these conditions, we also observed a significant decrease in apical aquaporin-2 immunolabeling in CD, with a cortico-medullary gradient, suggesting that K17F-induced diuresis could be linked to a direct action of apelin on CD. We then examined the potential cross talk between V1a AVP receptor (V1a-R), V2 AVP receptor (V2-R) and ApelinR signaling pathways in outer medullary CD (OMCD) and inner medullary CD microdissected rat CD. In OMCD, expressing the 3 receptors, K17F inhibited cAMP production and Ca2+ influx induced by 1-desamino-8-D-arginine vasopressin a V2-R agonist. Similar effects were observed in inner medullary CD expressing only V2-R and ApelinR. In contrast, in OMCD, K17F increased by 51% the Ca2+ influx induced by the stimulation of V1a-R by AVP in the presence of the V2-R antagonist SR121463B, possibly enhancing the physiological antagonist effect of V1a-R on V2-R. Thus, the diuretic effect of apelin is not only due to a central effect by inhibiting AVP release in the blood circulation as previously shown but also to a direct action of apelin on CD, by counteracting the antidiuretic effect of AVP occurring via V2-R.

scholarly journals Adrenomedullin Inhibits Osmotic Water Permeability in Rat Inner Medullary Collecting Ducts

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2533
Author(s):  
Fuying Ma ◽  
Guangping Chen ◽  
Eva L. Rodriguez ◽  
Janet D. Klein ◽  
Jeff M. Sands ◽  
...  
Keyword(s):  
Water Permeability ◽  
Collecting Duct ◽  
Osmotic Water Permeability ◽  
Water Reabsorption ◽  
Kinase C ◽  
Osmotic Water ◽  
Collecting Ducts ◽  
Medullary Collecting Duct ◽  
Camp Levels ◽  
Reduced Water

Adrenomedullin (ADM) is a vasodilator that causes natriuresis and diuresis. However, the direct effect of ADM on osmotic water permeability in the rat inner medullary collecting duct (IMCD) has not been tested. We investigated whether ADM and its ADM receptor components (CRLR, RAMP2, and 3) are expressed in rat inner medulla (IM) and whether ADM regulates osmotic water permeability in isolated perfused rat IMCDs. The mRNAs of ADM, CRLR, and RAMP2 and 3 were detected in rat IM. Abundant protein of CRLR and RAMP3 were also seen but RAMP2 protein level was extremely low. Adding ADM (100 nM) to the bath significantly decreased osmotic water permeability. ADM significantly decreased aquaporin-2 (AQP2) phosphorylation at Serine 256 (pS256) and increased it at Serine 261 (pS261). ADM significantly increased cAMP levels in IM. However, inhibition of cAMP by SQ22536 further decreased ADM-attenuated osmotic water permeability. Stimulation of cAMP by roflumilast increased ADM-attenuated osmotic water permeability. Previous studies show that ADM also stimulates phospholipase C (PLC) pathways including protein kinase C (PKC) and cGMP. We tested whether PLC pathways regulate ADM-attenuated osmotic water permeability. Blockade of either PLC by U73122 or PKC by rottlerin significantly augmented the ADM-attenuated osmotic water permeability and promoted pS256-AQP2 but did change pS261-AQP2. Inhibition of cGMP by L-NAME did not change AQP2 phosphorylation. In conclusion, ADM primarily binds to the CRLR-RAMP3 receptor to initiate signaling pathways in the IM. ADM reduced water reabsorption through a PLC-pathway involving PKC. ADM-attenuated water reabsorption may be related to decreased trafficking of AQP2 to the plasma membrane. cAMP is not involved in ADM-attenuated osmotic water permeability.

scholarly journals Reduced AQP1, -2, and -3 levels in kidneys of rats with CRF induced by surgical reduction in renal mass

1998 ◽  
Vol 275 (5) ◽  
pp. F724-F741 ◽  
Author(s):  
Tae-Hwan Kwon ◽  
Jørgen Frøkiaer ◽  
Mark A. Knepper ◽  
Søren Nielsen
Keyword(s):  
Urine Output ◽  
Renal Mass ◽  
Collecting Duct ◽  
Free Water ◽  
Urine Osmolality ◽  
Urinary Concentration ◽  
Water Reabsorption ◽  
Similar Reduction ◽  
Urine Production ◽  
Quantitative Immunoblotting

Urinary concentration characteristically decreases in response to a reduction in renal mass in chronic renal failure (CRF). In the present study, we examined whether there are changes in the expression of aquaporins in rats where CRF was induced by 5/6 nephrectomy. Plasma creatinine levels were significantly elevated consistent with significant CRF: 135.7 ± 15.1 ( n = 17, CRF) vs. 33.9 ± 1.1 μmol/l ( n = 11, sham), P < 0.05. Two weeks after 5/6 nephrectomy, the remnant kidneys were hypertrophied, and total renal mass increased to 65 ± 3% of sham levels ( P < 0.05). Urine production increased markedly from 40 ± 2 to 111 ± 3 μl ⋅ min−1 ⋅ kg−1in CRF rats ( P < 0.05), whereas urine osmolality and solute-free water reabsorption decreased significantly. Quantitative immunoblotting of total kidney membrane fractions revealed a significant decrease in total kidney AQP2 expression in CRF rats to 43 ± 12% of sham levels ( P < 0.05). A similar reduction was observed for AQP1 and AQP3. Furthermore, the increased urine output and decreased urine osmolality persisted in CRF rats despite 7 days treatment with 1-desamino-[8-d-arginine]vasopressin (DDAVP, 0.1 μg/h sc) compared with untreated sham-operated controls. Also, there was no change in AQP2 expression (which remained at 38 ± 3% of sham levels, P < 0.05), urine output, or urine osmolality between CRF rats with or without DDAVP treatment. Immunocytochemistry confirmed the decreased AQP2 expression in collecting duct principal cells in CRF rats, with a predominant apical labeling. In conclusion, the results demonstrated that there was a significant vasopressin-resistant downregulation of AQP2 and AQP3 as well as downregulation of AQP1 associated with the polyuria in CRF rats.

Water reabsorption by papillary collecting ducts in the remnant kidney

1982 ◽  
Vol 242 (6) ◽  
pp. F657-F663
Author(s):  
J. P. Pennell ◽  
J. J. Bourgoignie
Keyword(s):  
Collecting Duct ◽  
Sham Operation ◽  
Water Delivery ◽  
Water Reabsorption ◽  
Urinary Osmolality ◽  
Load Dependence ◽  
Physiological Processes ◽  
Collecting Ducts ◽  
Papillary Collecting Duct ◽  
Remnant Kidney

Water transport by terminal papillary collecting ducts was examined by micropuncture of the renal papilla in 15 rats with a solitary remnant kidney (RK) and in 27 normal rats, 10 of which had undergone sham operation. Before papillary exposure, urinary osmolality was significantly (P less than 0.001) lower in RK rats (685 vs. 1,722 mosmol/kg H2O in normal rats). After papillary exposure, urinary osmolality decreased by 50% in normal rats but did not change in RK rats. In RK rats, a greater percentage of filtered water was delivered to (5.74% vs. 2.29% in normal rats, P less than 0.001) and reabsorbed by (1.94% vs. 0.94% in normal rats, P less than 0.005) the terminal millimeter of papillary collecting ducts. Fractional water reabsorption by terminal papillary collecting ducts correlated directly (r = 0.83, P less than 0.001) with fractional water delivery, suggesting load dependence of water reabsorption. Estimated absolute water reabsorption by terminal collecting ducts was equivalent for remnant and normal kidneys and increased two-to fourfold in remnant kidneys when analyzed per functioning papillary collecting duct. There was an inverse relationship between urinary osmolality and fractional water delivery to papillary collecting ducts (r = 0.65, P less than 0.001). Although the data do not exclude functional alterations of papillary collecting ducts, the events underlying the reduction of urinary osmolality in remnant kidneys appear to involve physiological processes based on a high delivery and reabsorption of water.

Arginine vasopressin modulates expression of neuronal NOS in rat renal medulla

2002 ◽  
Vol 283 (3) ◽  
pp. F559-F568 ◽  
Author(s):  
Pierre-Yves Martin ◽  
Mathieu Bianchi ◽  
Frank Roger ◽  
Laurent Niksic ◽  
Eric Féraille
Keyword(s):  
Arginine Vasopressin ◽  
Collecting Duct ◽  
Duct System ◽  
Water Reabsorption ◽  
Enos Expression ◽  
Outer Medulla ◽  
Expression Levels ◽  
Principal Cells ◽  
Nos Isoforms ◽  
Nnos Expression

Arginine vasopressin (AVP) plays a central role in water balance. In principal cells of the collecting duct system, AVP controls the expression of several genes, including aquaporin-2. Because nitric oxide (NO) participates in the regulation of water reabsorption by the collecting duct system, we analyzed the effect of AVP on the expression of NO synthase (NOS) isoforms in the kidney. Rats were either water restricted or water loaded to modify the circulating AVP levels, and expressions of NOS isoforms were assessed by Western blot analysis. In water-restricted rats, endothelial NOS (eNOS) expression increased in the outer medulla, and neuronal NOS (nNOS) expression rose in both the outer medulla and the papilla. Conversely, water loading induced a decrease in expression of nNOS in the outer medulla and papilla but did not alter eNOS expression. Oral administration of the specific V2-receptor antagonist SR-121463B decreased nNOS expression in the outer medulla and papilla but did not alter eNOS expression levels. Finally, the very low nNOS expression levels observed in AVP-deficient Brattleboro rats was restored by AVP infusion for 1 wk. Thus AVP specifically increases nNOS expression levels in the renal outer medulla and papilla. Because nNOS is specifically expressed in principal cells of the collecting duct system, the stimulation of nNOS expression by AVP may participate in the control of water reabsorption.

Tubular prostaglandin E2 production and its role in urinary hypotonicity after release of ureteral occlusion in the rat

1987 ◽  
Vol 73 (4) ◽  
pp. 395-399 ◽  
Author(s):  
Shozo Torikai
Keyword(s):  
Prostaglandin E2 ◽  
Collecting Duct ◽  
Urine Osmolality ◽  
Urine Concentration ◽  
Pge2 Production ◽  
Endogenous Prostaglandin ◽  
Collecting Ducts ◽  
Ureteral Occlusion

1. In order to explore the involvement of endogenous prostaglandin E2 (PGE2) in the urine concentration defect after ureteral occlusion, PGE2 production by isolated collecting ducts in vitro and effects of indomethacin on urine osmolality in vivo were examined. 2. Twenty-four hours ureter obstruction caused increased PGE2 production by the medullary collecting ducts, which was maintained at a high level on the day after release of obstruction (0.8 ± 0.2 pg/mm normal, 8.1 ± 0.9 pg/mm 24 h obstruction, and 6.6 ± 1.0 pg/mm post-obstruction, mean ± sem). An enhanced PGE2 production was also observed for papillary collecting duct on the day after release of 24 h ureteral occlusion (3.9 ± 0.5 pg/mm normal and 7.7 ± 1.2 pg/mm post-obstruction). 3. Administration of indomethacin to the unilateral post-obstructive rats slightly raised the urine osmolality of the post-obstructed kidney (from 339 ± 17 to 390 ± 22 mosmol/kg H2O), while it had a greater effect on the contralateral intact kidney (from 1569 ± 138 to 2567 ± 198 mosmol/kg H2O). 4. Our data may indicate that the urine concentration defect after 24 h ureteral occlusion is ascribable mainly to a mechanism other than increased endogenous PGE2.

scholarly journals Race, sex, and the regulation of urine osmolality: observations made during water deprivation

2010 ◽  
Vol 299 (3) ◽  
pp. R977-R980 ◽  
Author(s):  
Michael L. Hancock ◽  
Daniel G. Bichet ◽  
George J. Eckert ◽  
Lise Bankir ◽  
Mary Anne Wagner ◽  
...  
Keyword(s):  
Water Conservation ◽  
Water Deprivation ◽  
Collecting Duct ◽  
Urine Osmolality ◽  
Thick Ascending Limb ◽  
Race Difference ◽  
Water Reabsorption ◽  
Blacks And Whites ◽  
Relationship Of ◽  
The Relationship

A more concentrated urine is excreted by blacks than whites and by men than women. The purpose of this study was to explore the physiological bases for the race and sex effects during water deprivation when osmoregulation is challenged and differences are amplified. Drinking water was withheld from 17 blacks (10 men) and 19 whites (9 men) for 24 h. Vasopressin (VP) levels and osmolality in plasma (Posmol) and urine (Uosmol) were measured basally and then every 4 h. Uosmol was higher in blacks at baseline ( P = 0.01) and during water deprivation ( P = 0.046). Before and during water deprivation, no differences were seen in levels of VP, Posmol, or the VP-Uosmol relationship between blacks and whites. Although VP levels were initially higher in men ( P < 0.02 for samples collected over the first 12 h), over the last 12 h of water deprivation, Uosmol was higher ( P = 0.027) and more responsive to the level of VP (in terms of slopes, P = 0.0001) in women than men. Our results suggest that, after a period of water deprivation, there develops a sensitivity of the collecting duct to VP that is greater in women. Although Uosmol is higher in blacks, the race difference in water conservation did not appear to result from differences in the level of VP or the sensitivity of the collecting duct to VP. Upstream effects such as Na+ uptake in the thick ascending limb, with its ensuing effects on water reabsorption, need to be considered in future studies of the relationship of race to water conservation.

Decreased vasopressin-mediated renal water reabsorption in rats with chronic aldosterone-receptor blockade

2000 ◽  
Vol 278 (2) ◽  
pp. F246-F256 ◽  
Author(s):  
Thomas E. N. Jonassen ◽  
Dominique Promeneur ◽  
Sten Christensen ◽  
Jørgen S. Petersen ◽  
Søren Nielsen
Keyword(s):  
Collecting Duct ◽  
Water Channel ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Receptor Blockade ◽  
Water Reabsorption ◽  
Aldosterone Receptor ◽  
Duct Ligation ◽  
Urine Production ◽  
Daily Urine

Previous studies have suggested that mineralocorticoids are needed for a normal action of vasopressin on collecting duct osmotic water permeability. However, the mechanisms behind this are unknown. To investigate if aldosterone-receptor blockade influences vasopressin type 2 receptor (V2)-mediated renal water reabsorption and the renal expression of the vasopressin-regulated water channel aquaporin-2 (AQP2), rats were treated with the aldosterone-receptor antagonist canrenoate (20 mg/day iv) for 4 wk. Daily urine flow was increased significantly by 44%, and urine osmolality was decreased by 27% in canrenoate-treated rats. Acute V2-receptor blockade (OPC-31260, 800 μg ⋅ kg−1 ⋅ h−1) was performed under conditions in which volume depletion was prevented. In control rats, OPC-31260 induced a significant increase in urine flow rate (V, +25%) and free water clearance ([Formula: see text], −29%). In canrenoate-treated rats, the effect of OPC-31260 was significantly reduced, and semiquantiative immunoblotting demonstrated a significant reduction (45%) in AQP2 expression. Because rats with common bile duct ligation (CBL) have a reduced vasopressin-mediated water reabsorption compared with normal rats (V: −24%;[Formula: see text]: −28%, and 86% downregulation of AQP2), the effect of canrenoate combined with OPC-31260 was tested. Canrenoate treatment of CBL rats significantly increased daily urine flow, decreased urine osmolality, and impaired the aquaretic response to OPC-31260 (V: −23%;[Formula: see text]: −31%) with maintained suppression of the renal AQP2 expression. Thus canrenoate treatment of normal and CBL rats showed 1) increased urine production, 2) reduced aquaretic effect of acute V2-receptor blockade, and 3) a marked reduction in AQP2 expression. This strongly supports the view that aldosterone plays a significant role for vasopressin-mediated water reabsorption.

scholarly journals Fluconazole Increases Osmotic Water Transport in Renal Collecting Duct through Effects on Aquaporin-2 Trafficking

2019 ◽  
Vol 30 (5) ◽  
pp. 795-810 ◽  
Author(s):  
Tanja Vukićević ◽  
Christian Hinze ◽  
Sandrine Baltzer ◽  
Nina Himmerkus ◽  
Catarina Quintanova ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Diabetes Insipidus ◽  
Nephrogenic Diabetes Insipidus ◽  
Collecting Duct ◽  
Urinary Output ◽  
Membrane Localization ◽  
Water Reabsorption ◽  
Principal Cells ◽  
Plasma Membrane Localization ◽  
Collecting Ducts

BackgroundArginine-vasopressin (AVP) binding to vasopressin V2 receptors promotes redistribution of the water channel aquaporin-2 (AQP2) from intracellular vesicles into the plasma membrane of renal collecting duct principal cells. This pathway fine-tunes renal water reabsorption and urinary concentration, and its perturbation is associated with diabetes insipidus. Previously, we identified the antimycotic drug fluconazole as a potential modulator of AQP2 localization.MethodsWe assessed the influence of fluconazole on AQP2 localization in vitro and in vivo as well as the drug's effects on AQP2 phosphorylation and RhoA (a small GTPase, which under resting conditions, maintains F-actin to block AQP2-bearing vesicles from reaching the plasma membrane). We also tested fluconazole's effects on water flow across epithelia of isolated mouse collecting ducts and on urine output in mice treated with tolvaptan, a VR2 blocker that causes a nephrogenic diabetes insipidus–like excessive loss of hypotonic urine.ResultsFluconazole increased plasma membrane localization of AQP2 in principal cells independent of AVP. It also led to an increased AQP2 abundance associated with alterations in phosphorylation status and ubiquitination as well as inhibition of RhoA. In isolated mouse collecting ducts, fluconazole increased transepithelial water reabsorption. In mice, fluconazole increased collecting duct AQP2 plasma membrane localization and reduced urinary output. Fluconazole also reduced urinary output in tolvaptan-treated mice.ConclusionsFluconazole promotes collecting duct AQP2 plasma membrane localization in the absence of AVP. Therefore, it might have utility in treating forms of diabetes insipidus (e.g., X-linked nephrogenic diabetes insipidus) in which the kidney responds inappropriately to AVP.

Furosemide action on collecting ducts: effect of prostaglandin synthesis inhibition

1983 ◽  
Vol 244 (6) ◽  
pp. F666-F673 ◽  
Author(s):  
D. R. Wilson ◽  
U. Honrath ◽  
H. Sonnenberg
Keyword(s):  
Collecting Duct ◽  
Prostaglandin Synthesis ◽  
Water Reabsorption ◽  
Inner Medullary Collecting Duct ◽  
Nephron Segments ◽  
Inhibit Prostaglandin Synthesis ◽  
Collecting Ducts ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Medullary Collecting Duct ◽  
Furosemide Administration

The effect of furosemide on inner medullary collecting duct chloride reabsorption has not been determined, and the blunting of furosemide action by drugs that inhibit prostaglandin synthesis, while known to occur, has not been examined in detail. The effect of indomethacin and meclofenamate on furosemide diuresis was studied in the rat using clearance and collecting duct microcatheterization methods. Furosemide-treated control animals showed complete inhibition of chloride, sodium, and water reabsorption in the inner medullary collecting duct. Rats given indomethacin or meclofenamate before and during furosemide administration showed marked reduction of the chloriuresis, natriuresis, and diuresis. Reduced delivery of sodium and chloride to the beginning of the inner medullary collecting duct, associated with a decrease in glomerular filtration rate and increased reabsorption in more proximal nephron segments, was largely responsible for the reduced natriuresis and chloriuresis during inhibition of prostaglandin synthesis. In addition, indomethacin increased collecting duct NaCl reabsorption toward normal, but meclofenamate showed no such effect. The results indicate that furosemide inhibits medullary collecting duct reabsorption of chloride, sodium, and water in the rat. The blunting of diuretic action seen with inhibition of prostaglandin synthesis is largely, although not entirely, due to effects of indomethacin and meclofenamate on furosemide action at nephron sites proximal to the collecting duct.

Effect of Carbamazepine on Plasma and Urine Arginine-Vasopressin

1978 ◽  
Vol 54 (4) ◽  
pp. 419-424 ◽  
Author(s):  
T. H. Thomas ◽  
S. G. Ball ◽  
J. K. Wales ◽  
M. R. Lee
Keyword(s):  
Drug Treatment ◽  
Arginine Vasopressin ◽  
Water Deprivation ◽  
Direct Action ◽  
Control Period ◽  
Urine Osmolality ◽  
Normal Subjects ◽  
Plasma Sodium ◽  
Sodium Plasma

1. Five normal subjects were studied before and during treatment with carbamazepine. 2. Plasma sodium, plasma and urine arginine-vasopressin and urine osmolality were measured during a day of water deprivation, before and during drug treatment. 3. During treatment with carbamazepine plasma sodium increased whereas plasma and urine arginine-vasopressin and urine osmolality decreased. Plasma and urine arginine-vasopressin were significantly correlated with urine osmolality. However, carbamazepine did not affect the osmolality of urine produced by the kidney, in response to endogenous arginine-vasopressin. 4. Plasma and urine arginine-vasopressin were significantly correlated with plasma sodium on both control and drug-treatment days, but the relationships of plasma and urine arginine-vasopressin to plasma sodium were different during carbamazepine treatment, as compared with the control period. 5. It is suggested that the threshold of the hypothalamic osmoreceptors for release of arginine-vasopressin is modified by carbamazepine, and that this may be either a direct action or secondary to another action of the drug.

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