Triiodothyronine enhances renal response to aldosterone in the rabbit collecting tubule.

Barlet, C.; Doucet, Alain

doi:10.1172/jci112858

Cited by 20 publications

(8 citation statements)

References 22 publications

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“…However, observation of this stimulatory effect required the presence of T3, as expected from previous in vivo studies (10,22). Indeed, it has been reported that the development of both antinatriuresis (22) and stimulation of collecting tubule Na' ,K+-ATPase (10) required lower doses of mineralocorticoids in euthyroid than in hypothyroid animals.…”

Section: Discussionsupporting

confidence: 55%

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Sodium-independent in vitro induction of Na+,K+-ATPase by aldosterone in renal target cells: permissive effect of triiodothyronine.

Barlet-Bas

Khadouri

Marsy

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

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The aim of this study was to develop an in vitro system in which we could study the causal relationship between short-term stimulation of Na' ,K+-ATPase in the collecting tubule by aldosterone on the one hand and protein synthesis and changes in intracellular Na+ concentration on the other hand. Previous in vivo studies suggested that triiodothyronine might facilitate aldosterone-induced stimulation of Na +,K + -ATPase. Results show that when segments of cortical collecting tubules microdissected from collagenase-treated kidneys of adrenalectomized rats were incubated for 3 hr in the presence of either 10-8 M aldosterone or 10'8 M triiodothyronine alone Na + ,K + -ATPase activity was not altered, whereas the addition of both hormones markedly stimulated the activity and the number of catalytic sites of Na+,K+-ATPase. This stimulation was abolished by actinomycin D and cycloheximide, whereas it was not altered in the absence of extraceliular sodium or in the presence of the luminal Na+-channel blocker amiloride. Thus, triiodothyronine facilitates the in vitro induction of Na+,K+-ATPase synthesis by aldosterone. Aldosterone action on Na+,K+-ATPase is independent of Na+ availability.The collecting tubule of the mammalian nephron is a major site of action of aldosterone, which stimulates Na+ reabsorption. In these cells, Na+ reabsorption from the luminal fluid to the peritubular medium is accomplished through a passive luminal entry by means of amiloride-sensitive channels and an active basolateral extrusion catalyzed by Na+,K+-ATPase. In vivo studies indicate that Na+ channels and also Na+,K+-ATPase are stimulated by aldosterone. Indeed, it has been reported previously that in vivo injection of aldosterone to adrenalectomized rats or rabbits stimulates Na+,K+-ATPase activity in the collecting tubule (1-3). However, we had been unable to reproduce this effect in vitro. Similarly, pieces of evidence for the in vitro effect of aldosterone on Na+ transport by the isolated microperfused collecting tubule in mammals are sparse and contradictory (4)(5)(6), in contrast to what is observed in vivo after administration of mineralocorticoids (5,(7)(8)(9). Because we recently demonstrated that triiodothyronine (T3) potentiates in vivo aldosterone action on the collecting tubule (10), we evaluated whether T3 might be the missing factor in in vitro induction of Na+ ,K +-ATPase by aldosterone. Indeed, incubation of single microdissected rat cortical collecting tubules (CCT) with both aldosterone and T3 markedly stimulated Na' ,K+-ATPase activity within 1-3 hr.The development of this in vitro system allowed us to further study the mechanisms underlying the stimulation of Na+,K+-ATPase by aldosterone in the rat collecting tubule. In particular, we investigated whether this stimulation is a primary action of aldosterone or whether it is secondary to the increment of intracellular Na+ concentration brought about by the rise of luminal Na+ permeability (11,12). For this purpose, we evaluated the actions of protein synthesis in...

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Section: Discussionsupporting

confidence: 55%

“…The incubation solution, derived from Eagle's minimal essential medium, contained 120 mM NaCl, 5 mM KCI, 1 mM CaC12, 1 mM MgSO4, 4 mM NaH2PO4, 4 mM NaHCO3, 5 mM glucose, 10 bules.…”

Section: Methodsmentioning

confidence: 99%

Sodium-independent in vitro induction of Na+,K+-ATPase by aldosterone in renal target cells: permissive effect of triiodothyronine.

Barlet-Bas

Khadouri

Marsy

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

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“…Similarly, thyroid hormone has been shown to increase the sensitivity of the effect of aldosterone to stimulate the Na-K-ATPase in the cortical collecting duct (37). Furthermore, there are now >20 claudin isoforms, and it is possible that thyroid hormone affects the maturation of another isoform.…”

Section: Discussionmentioning

confidence: 99%

Developmental Changes in Proximal Tubule Tight Junction Proteins

et al. 2005

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We demonstrated previously that neonatal proximal tubules have a lower passive paracellular permeability to chloride ions and higher resistance than that of adult proximal tubules. In addition, administration of thyroid hormone to neonates, before the normal maturational increase in serum thyroid hormone levels, prematurely accelerates the developmental increase in chloride permeability to adult levels. To test the hypothesis that there is a maturational change in tight junction proteins and that thyroid hormone mediates these changes, we examined the two known tight junction proteins present in proximal tubules, occludin and claudin 2. Using immunoblot and immunohistochemistry, we demonstrated that claudin 2 has a 4-fold greater abundance in neonatal proximal tubules than in adult tubules. Occludin, however, has a 4-fold greater expression in adult tubules than in neonatal tubules. Administration of thyroid hormone to neonates did not affect claudin 2 expression, occludin expression, or the transepithelial resistance in rat proximal tubule cells in vitro. In conclusion, there are postnatal maturational changes in tight junction proteins. The factors that cause these maturational changes are unknown but unlikely to be due solely to the maturational increase in thyroid hormone.The proximal tubule receives an ultrafiltrate from the glomerulus and reabsorbs two thirds of the ultrafiltrate in a nearly iso-osmotic manner. In addition to active transcellular fluid transport, the proximal tubule reabsorbs solutes via passive diffusion across the paracellular pathway. The early proximal tubule reabsorbs glucose and amino acids and preferentially reabsorbs bicarbonate over chloride ions (1,2), which leaves the luminal fluid delivered to the late proximal tubule with a higher chloride concentration and lower bicarbonate concentration than that in the peritubular plasma (1,2). Passive solute transport is dependent on the gradients that develop between lumen and peritubular capillary and permeability properties of the paracellular pathway.Approximately two thirds of the filtered chloride is reabsorbed by the adult proximal tubule (1,3 active and transcellular and half is passive and paracellular (3-5). Active NaCl transport is mediated by the parallel operation of the Na+/H+ exchanger and a Cl−/base exchanger (3,4). Passive Cl absorption is mediated by diffusion of chloride ions down its concentration gradient generated in the early proximal tubule (6,7). Thus, the permeability properties of the paracellular pathway can affect a significant amount of proximal tubule NaCl transport.Furthermore, the permeability properties of the paracellular pathway serve as a barrier to prevent the back diffusion of glucose, amino acids, phosphate, bicarbonate, and other solutes that are in higher concentration in the peritubular fluid than in the lumen of the late proximal tubule. In previous in vitro rabbit microperfusion studies, our laboratory demonstrated that unlike the adult segment, the neonatal proximal tubule was impermeab...

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“…This probably is also the site of highest transcript levels of Dio1 in rat kidney (49). Furthermore, aldosterone-induced Na ϩ -K ϩ -ATPase activity in the distal tubule is markedly diminished after thyroidectomy (6). These and other evidence (4,18,44) point to direct endocrine cross talk between thyroid hormone signaling and the activity of the RAAS.…”

Section: Discussionmentioning

confidence: 75%

V2 vasopressin receptor deficiency causes changes in expression and function of renal and hypothalamic components involved in electrolyte and water homeostasis

Schliebe¹,

Strotmann²,

Busse³

et al. 2008

American Journal of Physiology-Renal Physiology

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August 20, 2008; doi:10.1152/ajprenal.00465.2007.-Polyuria, hypernatremia, and hypovolemia are the major clinical signs of inherited nephrogenic diabetes insipidus (NDI). Hypernatremia is commonly considered a secondary sign caused by the net loss of water due to insufficient insertion of aquaporin-2 water channels into the apical membrane of the collecting duct cells. In the present study, we employed transcriptome-wide expression analysis to study gene expression in V2 vasopressin receptor (Avpr2)-deficient mice, an animal model for X-linked NDI. Gene expression changes in NDI mice indicate increased proximal tubular sodium reabsorption. Expression of several key genes including Na ϩ -K ϩ -ATPase and carbonic anhydrases was increased at the mRNA levels and accompanied by enhanced enzyme activities. In addition, altered expression was also observed for components of the eicosanoid and thyroid hormone pathways, including cyclooxygenases and deiodinases, in both kidney and hypothalamus. These effects are likely to contribute to the clinical NDI phenotype. Finally, our data highlight the involvement of the renin-angiotensin-aldosterone system in NDI pathophysiology and provide clues to explain the effectiveness of diuretics and indomethacin in the treatment of NDI. vasopressin receptor; diabetes insipidus; G protein-coupled receptor; signal transduction; hypernatremia THE NEUROHYPOPHYSEAL PEPTIDE arginine vasopressin (AVP) is an essential hormone in mammals that regulates the body's water and electrolyte homeostasis. AVP mediates its renal actions through activation of the tubular V2 vasopressin receptor (Avpr2). Avpr2 stimulation activates the G s protein/adenylyl cyclase signaling cascade and eventually results in the insertion of the water channel protein aquaporin-2 (AQP2) into the apical plasma membrane of the collecting duct cells (42). The major physiological importance of the AVP regulatory system becomes apparent when key components are defective. AVP deficiency results in central diabetes insipidus (CDI), whereas inactivating mutations in Avpr2 or AQP2 genes lead to inherited forms of nephrogenic diabetes insipidus (NDI). In NDI, the renal concentrating capability is impaired and the kidney produces large volumes of hypotonic urine, a situation that may lead to severe dehydration and electrolyte imbalance, in particular hypernatremia and hyperchloremia (29). Mechanistically, hypernatremia is believed to be the result of net water depletion. This assumption is supported by effective treatment of NDI patients with abundant water intake. Current therapy of NDI patients further includes a low-sodium diet and thiazide diuretics, often in combination with the potassium-sparing diuretic amiloride.Thiazide diuretics [e.g., hydrochlorothiazide (HCTZ)] paradoxically decrease urine volume and increase urine osmolality in NDI patients (21). A recent study (40) showed upregulation of AQP2 and a number of distal renal Na ϩ transporters, such as the thiazide-sensitive NaCl cotransporter (NCC) and the epithelial sodiu...

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Triiodothyronine enhances renal response to aldosterone in the rabbit collecting tubule.

Cited by 20 publications

References 22 publications

Sodium-independent in vitro induction of Na+,K+-ATPase by aldosterone in renal target cells: permissive effect of triiodothyronine.

Sodium-independent in vitro induction of Na+,K+-ATPase by aldosterone in renal target cells: permissive effect of triiodothyronine.

Developmental Changes in Proximal Tubule Tight Junction Proteins

V2 vasopressin receptor deficiency causes changes in expression and function of renal and hypothalamic components involved in electrolyte and water homeostasis

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