Angiotensin II Potentiates Vasopressin-Dependent cAMP Accumulation in CHO Transfected Cells. Mechanisms of Cross-Talk Between AT1A and V2 Receptors

Klingler, Cécile; Ancellin, Nicolas; Barrault, Marie-Bénédicte; Morel, Alain; Buhler, Jean‐Marie; Elalouf, Jean‐Marc; Clauser, Éric; Lugnier, Claire; Corman, B.

doi:10.1016/s0898-6568(97)00077-6

Cited by 24 publications

(29 citation statements)

References 21 publications

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“…Since regulation of intracellular AQP2 trafficking, AQP2 protein expression, and osmotic water permeability in the collecting duct principal cells involves intracellular cAMP production and [Ca 2ϩ ] levels (9, 14, 52), we hypothesize that ANG II AT 1 receptor blockade could reduce the synergetic effects of ANG II on the vasopressin-induced increase in intracellular cAMP and [Ca 2ϩ ] levels. This hypothesis was further supported by previous in vitro studies demonstrating cross talk between the signaling pathways of vasopressin and ANG II (23,30). Consistent with this, we found that inner medullary expression of AQP2 and p-AQP2 and urine osmolality were not increased in response to long-term DDAVP administration in NaCl-restricted rats in the presence of AT 1 receptor blocker candesartan cotreatment.…”

Section: Occupation Of Ang II At 1 Receptor Plays a Role In Regulatiosupporting

confidence: 91%

Angiotensin II AT₁receptor blockade decreases vasopressin-induced water reabsorption and AQP2 levels in NaCl-restricted rats

Kwon

Nielsen²,

Knepper³

et al. 2005

American Journal of Physiology-Renal Physiology

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Kwon, Tae-Hwan, Jakob Nielsen, Mark A. Knepper, Jørgen Frøkiaer, and Søren Nielsen. Angiotensin II AT 1 receptor blockade decreases vasopressin-induced water reabsorption and AQP2 levels in NaCl-restricted rats. Am J Physiol Renal Physiol 288: F673-F684, 2005. First published December 7, 2004; doi:10.1152/ajprenal.00304. 2004.-Vasopressin and ANG II, which are known to play a major role in renal water and sodium reabsorption, are mainly coupled to the cAMP/PKA and phosphoinositide pathways, respectively. There is evidence for cross talk between these intracellular signaling pathways. We therefore hypothesized that vasopressin-induced water reabsorption could be attenuated by ANG II AT 1 receptor blockade in rats. To address this, three protocols were used: 1) DDAVP treatment (20 ng/h sc for 7 days, n ϭ 8); 2) DDAVP (20 ng/h sc for 7 days) and candesartan (1 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 sc for 7 days) cotreatment (n ϭ 8); and 3) vehicle infusion as the control (n ϭ 8). All rats were maintained on a NaCl-deficient diet (0.1 meq Na ϩ ⅐ 200 g body wt Ϫ1 ⅐ day Ϫ1 ) during the experiment. DDAVP treatment alone resulted in a significant decrease in urine output (3.1 Ϯ 0.2 ml/day) compared with controls (11.5 Ϯ 2.2 ml/day, P Ͻ 0.05), whereas the urine output was significantly increased in response to DDAVP and candesartan cotreatment (9.8 Ϯ 1.0 ml/day, P Ͻ 0.05). Consistent with this, rats cotreated with DDAVP and candesartan demonstrated decreased urine osmolality (1,319 Ϯ 172 mosmol/kgH2O) compared with rats treated with DDAVP alone (3,476 Ϯ 182 mosmol/kgH2O, P Ͻ 0.05). Semiquantitative immunoblotting revealed significantly decreased expression of medullary aquaporin-2 (AQP2) and AQP2 phosphorylated in the PKA phosphorylation consensus site Ser-256 (p-AQP2) in response to DDAVP and candesartan cotreatment compared with DDAVP treatment alone. In addition, cortical and medullary AQP1 was also downregulated. Fractional sodium excretion (FENa) and plasma potassium levels were markedly increased, and the expressions of the cortical type 3 Na ϩ /H ϩ exchanger (NHE3), thiazidesensitive Na-Cl cotransporter (NCC), and Na-K-ATPase were significantly decreased in response to DDAVP and candesartan cotreatment. Moreover, medullary type 1 bumetanide-sensitive Na-K-2Cl cotransporter expression showed a marked gel mobility shift from 160 to ϳ180 kDa corresponding to enhanced glycosylation, whereas expression was unchanged. In conclusion, ANG II AT 1 receptor blockade in DDAVP-treated rats was associated with decreased urine concentration and decreased AQP2 and AQP1 expression. Moreover, FENa was increased in parallel with decreased expression of NHE3, NCC, and Na-K-ATPase. These results suggest that ANG II AT1 receptor activation plays a significant role in regulating aquaporin and sodium transporter expression and modulating urine concentration in vivo.aquaporin; calcium; cAMP; type 1 bumetanide-sensitive Na-K-2Cl cotransporter; urine concentration VASOPRESSIN AND ANG II are importantly involved in the renal conservation of water and sodiu...

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Section: Occupation Of Ang II At 1 Receptor Plays a Role In Regulatiosupporting

confidence: 91%

Angiotensin II AT₁receptor blockade decreases vasopressin-induced water reabsorption and AQP2 levels in NaCl-restricted rats

Kwon

Nielsen²,

Knepper³

et al. 2005

American Journal of Physiology-Renal Physiology

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“…7, 8, and 10). The lack of adenylyl cyclase III and ERK1/2 responses to water deprivation or DDAVP in Agtr1a Ϫ/Ϫ mice is significant, because adenylyl cyclase III is expressed primarily in inner medulla collecting tubules and appears to mediate V 2 receptor-induced cAMP production in collecting duct cells (5,15,21,22). cAMP is the key second messenger that mediates the translocation of AQP2 from intracellular vesicles to apical membranes (10,11,22).…”

Section: Or In Agtr1amentioning

confidence: 99%

“…In animal studies, administration of physiological concentrations of ANG II decreased urine excretion and increased urine osmolality, and, conversely, chronic administration of angiotensin-converting enzyme inhibitors or AT 1 receptor blockers led to increased excretion of diluted urine (3,12,24,29). In vitro, ANG II stimulates the translocation of AQP2 from intracellular vesicles to cell membranes in cultured inner medullary collecting duct cells (25) or potentiates AVPinduced cAMP production and AQP2 expression in CHO cells coexpressing dual AT 1a and V 2 receptors (21). Furthermore, we and others (30,37) have recently shown that deletion of AT 1a receptors is associated with the development of polyuria and a urine-concentrating defect in AT 1a receptor-deficient (Agtr1a Ϫ/Ϫ ) mice.…”

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confidence: 97%

AT_1a receptor signaling is required for basal and water deprivation-induced urine concentration in AT_1a receptor-deficient mice

Shao

Zhuo

2012

American Journal of Physiology-Renal Physiology

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Li XC, Shao Y, Zhuo JL. AT1a receptor signaling is required for basal and water deprivation-induced urine concentration in AT 1a receptor-deficient mice. Am J Physiol Renal Physiol 303: F746-F756, 2012. First published June 27, 2012 doi:10.1152/ajprenal.00644.2011It is well recognized that ANG II interacts with arginine vasopressin (AVP) to regulate water reabsorption and urine concentration in the kidney. The present study used ANG II type 1a (AT 1a) receptor-deficient (Agtr1a Ϫ/Ϫ ) mice to test the hypothesis that AT 1a receptor signaling is required for basal and water deprivation-induced urine concentration in the renal medulla. Eight groups of wild-type (WT) and Agtr1a Ϫ/Ϫ mice were treated with or without 24-h water deprivation and 1-desamino-8-D-AVP (DDAVP; 100 ng/h ip) for 2 wk or with losartan (10 mg/kg ip) during water deprivation. Under basal conditions, Agtr1a Ϫ/Ϫ mice had lower systolic blood pressure (P Ͻ 0.01), greater than threefold higher 24-h urine excretion (WT mice: 1.3 Ϯ 0.1 ml vs. Agtr1a Ϫ/Ϫ mice: 5.9 Ϯ 0.7 ml, P Ͻ 0.01), and markedly decreased urine osmolality (WT mice: 1,834 Ϯ 86 mosM/kg vs. Agtr1a Ϫ/Ϫ mice: 843 Ϯ 170 mosM/kg, P Ͻ 0.01), without significant changes in 24-h urinary Na ϩ excretion. These responses in Agtr1a Ϫ/Ϫ mice were associated with lower basal plasma AVP (WT mice: 105 Ϯ 8 pg/ml vs. Agtr1a Ϫ/Ϫ mice: 67 Ϯ 6 pg/ml, P Ͻ 0.01) and decreases in total lysate and membrane aquaporin-2 (AQP2; 48.6 Ϯ 7% of WT mice, P Ͻ 0.001) and adenylyl cyclase isoform III (55.6 Ϯ 8% of WT mice, P Ͻ 0.01) proteins. Although 24-h water deprivation increased plasma AVP to the same levels in both strains, 24-h urine excretion was still higher, whereas urine osmolality remained lower, in Agtr1a Ϫ/Ϫ mice (P Ͻ 0.01). Water deprivation increased total lysate AQP2 proteins in the inner medulla but had no effect on adenylyl cyclase III, phosphorylated MAPK ERK1/2, and membrane AQP2 proteins in Agtr1a Ϫ/Ϫ mice. Furthermore, infusion of DDAVP for 2 wk was unable to correct the urine-concentrating defects in Agtr1a Ϫ/Ϫ mice. These results demonstrate that AT 1a receptor-mediated ANG II signaling is required to maintain tonic AVP release and regulate V2 receptormediated responses to water deprivation in the inner medulla. angiotensin II; angiotensin II type 1a receptor; adenylyl cyclases; aquaporin 2; arginine vasopressin; inner medullary collecting ducts; urine concentration WATER REABSORPTION by the inner medulla plays an important role in maintaining basal body electrolytes and fluid balance, urine concentration, and blood pressure homeostasis. Physiologically, water transport in the inner medulla is primarily regulated by the neuropeptide hormone arginine vasopressin ([Arg 8 ]-AVP), which is released from the posterior pituitary in response to changes in extracellular fluid volume and plasma and urine osmolality (1,23,40). In the inner medulla of the kidney, AVP binds to G s protein-coupled type 2 (V 2 ) receptors expressed on basolateral membranes of principal cells, which activates adenylyl cyclases ...

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“…The cells were incubated with complete buffer plus 1 µM AVP or 10 µM forskolin for 4 min at 37 C in presence of 5 µM indomethacin and 1 mM 3-isobutyl 1-methyl xanthine (IBMX) as described elsewhere (Klinger et al 1998). The cAMP content of each sample was measured by radioimmunoassay (cAMP kit, Immunotech, Marseille, France) according to the instructions of the manufacturer.…”

Section: Camp Productionmentioning

confidence: 99%

Gene and cDNA cloning and characterization of the mouse V3/V1b pituitary vasopressin receptor

Ventura

René²,

Keyzer³

et al. 1999

Journal of Molecular Endocrinology

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The gene of the mouse V3/V1b receptor was identified by homology cloning. One of the genomic clones contained the entire coding sequence. The cDNA presented high identity with rat (92%) and human (84%) sequences. Southern blot analysis indicated the existence of a single gene. Tissue distribution was studied by RT-PCR. The major site of expression was the pituitary. A faint signal was also present in hypothalamus, brain, adrenal, pancreas and colon. The mouse corticotroph cell line, AtT20, did not express the transcript. In order to confirm the identity of the sequence, the V3/V1b receptor cDNA was cloned and stably expressed in CHO-AA8 Tet-Off cells under the control of tetracycline. When transfected cells were treated with arginine vasopressin (AVP), inositol phosphate production increased in a dose-dependent manner, indicating that the V3/V1b receptor couples to phospholipase C. Moreover, AVP did not stimulate cAMP production. Binding studies with [3 H]AVP indicated that the affinity of the mouse V3/V1b receptor (K d =0·5 nM) is similar to that reported for rat and human receptors. The rank order of potency established in competition binding experiments with different analogues was representative of a V3/V1b profile, distinct from V1a and V2. However, significant differences were found between human and mouse receptors tested in parallel. Thus the pharmacology of V3/V1b receptors can not be transposed among different species.

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Angiotensin II Potentiates Vasopressin-Dependent cAMP Accumulation in CHO Transfected Cells. Mechanisms of Cross-Talk Between AT1A and V2 Receptors

Cited by 24 publications

References 21 publications

Angiotensin II AT₁receptor blockade decreases vasopressin-induced water reabsorption and AQP2 levels in NaCl-restricted rats

Angiotensin II AT₁receptor blockade decreases vasopressin-induced water reabsorption and AQP2 levels in NaCl-restricted rats

AT_1a receptor signaling is required for basal and water deprivation-induced urine concentration in AT_1a receptor-deficient mice

Gene and cDNA cloning and characterization of the mouse V3/V1b pituitary vasopressin receptor

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Angiotensin II Potentiates Vasopressin-Dependent cAMP Accumulation in CHO Transfected Cells. Mechanisms of Cross-Talk Between AT1A and V2 Receptors

Cited by 24 publications

References 21 publications

Angiotensin II AT1receptor blockade decreases vasopressin-induced water reabsorption and AQP2 levels in NaCl-restricted rats

Angiotensin II AT1receptor blockade decreases vasopressin-induced water reabsorption and AQP2 levels in NaCl-restricted rats

AT1a receptor signaling is required for basal and water deprivation-induced urine concentration in AT1a receptor-deficient mice

Gene and cDNA cloning and characterization of the mouse V3/V1b pituitary vasopressin receptor

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Angiotensin II AT₁receptor blockade decreases vasopressin-induced water reabsorption and AQP2 levels in NaCl-restricted rats

Angiotensin II AT₁receptor blockade decreases vasopressin-induced water reabsorption and AQP2 levels in NaCl-restricted rats

AT_1a receptor signaling is required for basal and water deprivation-induced urine concentration in AT_1a receptor-deficient mice