Two oxytocin-binding site subtypes in rat kidney: pharmacological characterization, ontogeny and localization by in vitro and in vivo autoradiography

Arpin-Bott, Marie-Pierre; Waltisperger, Elisabeth; Freund-Mercier, Marie José; Stoeckel, M. E.

doi:10.1677/joe.0.1530049

Cited by 23 publications

(15 citation statements)

References 15 publications

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“…The endogenous plasma concentrations of oxytocin in our anaesthetized rats were within the range achieved by doses of oxytocin previously shown to increase GFR (Forsling et al 1994, Windle et al 1997. Receptors for oxytocin have been located in the glomerulus (Stoeckel et al 1987) and the macula densa region of the tubule (Stoeckel & Freund-Mercier 1989, Arpin-Bott et al 1997, and it seems reasonable to propose that these might have mediated the observed change in GFR (the macula densa being intimately involved in the tubulo-glomerular feedback control of GFR; Briggs & Schnermann 1987).…”

Section: Resultssupporting

confidence: 66%

Contribution of endogenous oxytocin to sodium excretion in anaesthetized, surgically operated rats

Walter¹,

Forsling²,

Shirley³

2000

Journal of Endocrinology

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In order to determine the possible role of endogenous oxytocin in controlling electrolyte and water excretion in animals whose renal function is being assessed by invasive techniques, rats were anaesthetized and subjected to micropuncture surgery. Clearance measurements were made in the presence and absence of the potent oxyto- 9 ]-vasotocin. In rats infused with vehicle alone, glomerular filtration rate (GFR), sodium excretion and urine flow rate remained stable. In contrast, in antagonisttreated rats GFR was modestly reduced (P<0·05), and there were large falls in both absolute and fractional sodium excretion (P<0·01 in each case) and absolute and fractional water excretion (P<0·05 in each case), indicating effects on both filtered load and fractional tubular reabsorption.The antinatriuresis was not accompanied by a change in the fractional excretion of lithium, suggesting that proximal tubular function is unaffected by oxytocin receptor antagonism; nor was it accompanied by a change in the fractional excretion of potassium, suggesting that the tubular effect is located beyond the potassium secretory site, i.e. downstream of the cortical collecting tubule.We conclude that circulating plasma concentrations of oxytocin during anaesthesia and moderate surgery are sufficient to enhance GFR and reduce fractional tubular sodium and water reabsorption. This has important implications for the interpretation of invasive studies such as micropuncture.

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Section: Resultssupporting

confidence: 66%

Contribution of endogenous oxytocin to sodium excretion in anaesthetized, surgically operated rats

Walter¹,

Forsling²,

Shirley³

2000

Journal of Endocrinology

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“…11 In contrast, the contractile effect of OT on cultured myometrium cells was blocked by an OT receptor, but not V1 receptor, antagonist. 11 OT receptors have been identified in the kidney, 12 and OT has been shown to exert an antidiuretic effect in vasopressin-deficient Brattleboro rats 9,10 and to increase water transport in isolated IMCD. 8,9 These effects have been shown to be abolished by the administration of a V2 vasopressin receptor antagonist.…”

Section: Discussionmentioning

confidence: 99%

Molecular Mechanisms of Antidiuretic Effect of Oxytocin

Wang

Summer

et al. 2008

Journal of the American Society of Nephrology

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Oxytocin is known to have an antidiuretic effect, but the mechanisms underlying this effect are not completely understood. We infused oxytocin by osmotic minipump into vasopressin-deficient Brattleboro rats for five days and observed marked antidiuresis, increased urine osmolality, and increased solute-free water reabsorption. Administration of oxytocin also significantly increased the protein levels of aquaporin-2 (AQP2), phosphorylated AQP2 (p-AQP2), and AQP3 in the inner medulla and in the outer medulla plus cortex. Immunohistochemistry demonstrated increased AQP2 and p-AQP2 expression and trafficking to the apical plasma membrane of principal cells in the collecting duct, and increased AQP3 expression in the basolateral membrane. These oxytocin-induced effects were blocked by treatment with the vasopressin V2 receptor antagonist SR121463B, but not by treatment with the oxytocin receptor antagonist GW796679X. We conclude that vasopressin V2 receptors mediate the antidiuretic effects of oxytocin, including increased expression and apical trafficking of AQP2, p-AQP2, and increased AQP3 protein expression. 19: 225-232, 200819: 225-232, . doi: 10.1681 In recent years, the understanding of the molecular basis for the antidiuretic effect of vasopressin has been substantially advanced. The vasopressin V2 receptor 1 and renal aquaporin (AQP) water channels 2 have been cloned. Vasopressin has been shown to mediate both long-and short-term effects on AQP2 in the principal cells of the collecting duct. The long-term effect of vasopressin leads to increased expression of AQP2, whereas the shortterm effects involve trafficking of AQP2 to the apical membrane of the principal cells. 3 There is also evidence that vasopressin increases AQP3 protein expression on the basolateral membrane of the principal cells 4 and up-regulates the Na-K-2Cl cotransporter, 5 the initiator of the countercurrent concentrating mechanism. J Am Soc NephrolOxytocin (OT) is also known to possess antidiuretic properties. 6 In this regard, use of OT to induce labor in pregnancy has been associated with water retention and hyponatremia. 7 OT has been shown in vitro to increase osmotic water transport in microdissected renal inner medullary collecting ducts (IMCD) 8 and in vivo to cause an antidiuresis in vasopressin-deficient Brattleboro rats. 9,10 These effects were reversed by a vasopressin V2 receptor antagonist, suggesting that OT stimulation of vasopressin receptors mediates the antidiuresis. These in vitro observations were not altered by two different OT receptor antagonists. 8 The effect of OT on the long-and short-term regulation of AQP2 or the expression of AQP3 and Na-K-2Cl cotransporter has not been studied. The present study was therefore undertaken to advance the knowledge at the

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“…In the current work the oxytocin antagonist chosen appeared to have no such partial agonist effect, as indicated by stimulated cAMP production. It has been suggested that there could be two subtypes of oxytocin receptors in the kidney (Arpin-Bott et al 1997), and in the uterus, where GN-OVT inhibited both the uterotonic action and prostaglandin-releasing action of oxytocin, whereas [Pen',pMePheZ ,Thr4,0rns]oxytocin only inhibited the uterotonic action of oxytocin (Chan el al. 1993).…”

Section: Discussionmentioning

confidence: 99%

Separate receptors mediate oxytocin and vasopressin stimulation of cAMP in rat inner medullary collecting duct cells

Wargent

Burgess

Laycock³

et al. 1999

Experimental Physiology

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SUMMARYThe two neurohypophysial hormones arginine vasopressin (AVP) and oxytocin have actions in the inner medullary collecting duct (IMCD) where both peptides induce an increas8e in cAMP accumulation. The present study has employed a novel IMCD cell line to determine whether these two hormones induce cAMP accumulation via common or separate receptors, and to characterize the potential receptors responsible. Equal volumes of vehicle (150 mM NaCI) or hormone/antagonist solutions were added to aliquots of lo4 IMCD cells in the presence of M 3-isobutylmethylxanthine (IBMX) and incubated at 37OC for 4min. cAMP levels were determined by radioimmunoassay and protein concentration by Bradford assay. Both AVP and oxytocin elicited dose-dependent increases in cAMP generation, though oxytocin was less potenlt than AVP (EC,, = 1.6 x lo-' M vs. 7.4 x lo-'' M). AVP at lo-' M and oxytocin at M, concentrations sufficient to elicit near-maximal cAMP accumulation, resulted in cAMP levels of 73.4 k 1.7 and 69.0 k 3.3 pmol (mg protein)-' (4 min)-', respectively (n = lo), compared with the vehicle-treated basal value of 37.7 f 2.2 pmol (mg protein)-' (4 min)-' ( P c 0.001, n = 10). Combined AVP (lo-' M) and oxytocin M) resulted in cAMP accumulation of 63.8 f 3.1 pmol (mg protein)-' (4 min)-' (n = lo), which was not significantly different from the effect of oxytocin alone, but slightly less than that for AVP alone ( P c 0.05). A submaximal concentration of AVP (lo-" M) induced cAMP accumulation of 48.6 f 2.5 pmol (mg protein)-' (4 min)-' ( P c 0.01 compared with basal level of 34.9 f 2.4 pmol (mg protein)-' (4 min)-', n = lo), which was blocked in the presence of a vasopressin V, receptor antagonist M OPC-31260) but not by the oxytocin receptor antagonist ( low6 M [Pen',pMePhe2,Thr4,0rns]oxytocin) ( 3 6 3 k 6.1 and 45.1 f 1.3 pmol (mg protein)-' (4 min)-' respectively, P c 0.05, n = 10). A submaximal concentration of oxytocin M) induced a cAMP accumulation of 45.8 f 1.8 pmol (mg protein)-' (4 min)-' (n = lo), which was reduced by addition of M oxytocin antagonist (36.3 & 2.1 pmol (mg protein)-' (4 min)-', P c 0.05, n = lo), whereas co-incubation with M of the V, receptor antagonist had no effect (43.2 f 1.3 pmol (mg protein)-' (4 min)-', n = 10).These results indicate that AVP and oxytocin induce cAMP accumulation from a common ATP pool in IMCD cells, and that separate vasopressin V, and oxytocin receptor systems are involved, perhaps coupled to a common adenylate cyclase system. INTRODUCTIONThe antidiuretic osmotic water transport (P,) in the inner medullary collecting duct of most mammals, including humans and rats, is regulated by arginine vasopressin (A'VP) via CAMPmediated translocation of aquaporin-2-containing vesicles to the luminal membrane. The other neurohypophysial hormone, oxytocin, has also been demonstrated to have an antit Corresponding author: rnopleetw@stud.rnan.ac.uk , 1984;Lyness et al. 1985) and has also been found to stimulate an increase in osmotic water transport (P,) in microdissected inner medullary colle...

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Two oxytocin-binding site subtypes in rat kidney: pharmacological characterization, ontogeny and localization by in vitro and in vivo autoradiography

Cited by 23 publications

References 15 publications

Contribution of endogenous oxytocin to sodium excretion in anaesthetized, surgically operated rats

Contribution of endogenous oxytocin to sodium excretion in anaesthetized, surgically operated rats

Molecular Mechanisms of Antidiuretic Effect of Oxytocin

Separate receptors mediate oxytocin and vasopressin stimulation of cAMP in rat inner medullary collecting duct cells

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