Información del artículo
Resumen
Los antagonistas no peptídicos de la vasopresina (AVP), llamados vaptanes, se desarrollaron en la década de los noventa con el fin de antagonizar tanto su efecto presor como antidiurético.
Se distinguen 3 subtipos de receptores de la AVP: V1a, V1b y V2. Los primeros se hallan ampliamente distribuidos en el organismo, y las localizaciones en vasos y miocardio son las más destacadas. Los receptores V1b esencialmente están en la hipófisis anterior y median la liberación de corticotropina (ACTH). Por su parte, los receptores V2 se encuentran principalmente en las células del túbulo colector renal. Tanto los receptores V1a como V1b actúan a través del calcio (Ca++) intracelular. El receptor V2 actúa a través de la generación de adenosín monofosfato-3’,5’ cíclico (AMPc), que en último término genera la movilización de la aquaporina 2 (AQP2), que produce un aumento de la permeabilidad y permite la entrada de agua al interior de la célula.
Los vaptanes actúan de forma competitiva a nivel de receptor de la AVP. Los más importantes son mozavaptan, lixivaptan, satavaptan y tolvaptan, que son antagonistas selectivos V2 y se administran por vía oral. Conivaptan es un antagonista tanto de V1 como de V2 y su empleo es por vía intravenosa. Las características generales más importantes de todos ellos son su efecto sobre la eliminación únicamente de agua libre sin afectar la excreción de electrolitos. Hay diferentes estudios de todos ellos, tanto en estado de hiponatremia hipervolémica, como la insuficiencia cardíaca o cirrosis hepática, como en la normovolémica, como el síndrome de secreción inadecuada de hormona antidiurética (SIADH). Los estudios actuales muestran que los vaptanes son efectivos y bien tolerados, aunque las limitaciones se derivan de un conocimiento insuficiente de estos fármacos. No hay estudios de los vaptanes en cuadros de hiponatremia grave y no se han descrito cuadros de desmielinización osmótica por corrección excesiva de la hiponatremia.
Palabras clave:
Vasopresina
Hiponatremia
Receptor AVP
Antagonista del receptor
Abstract
The non-peptide vasopressin antagonists (VPA), called vaptans, were developed in the 1990s to antagonize both the pressor and antidiuretic effects of vasopressin.
There are three subtypes of VPA receptors: V1a, V1b and V2. V1a receptors are widely distributed in the body, mainly the blood vessels and myocardium. The V1b receptors are located mainly in the anterior pituitary gland and play a role in ACTH release. V2 receptors are located in the collecting tubular renal cells. Both V1a and V1b receptors act through the intracellular phosphoinositol signalling pathway, Ca++ being the second messenger. V2 receptors work through AMPc generation, which promotes aquaporin 2 (AQP2) trafficking and allows water to enter the cell.
The vaptans act competitively at the AVP receptor. The most important are mozavaptan, lixivaptan, satavaptan and tolvaptan, all of which are selective V2 antagonists and are administered through the oral route. In contrast, conivaptan is a dual V1 and V2 antagonist administered through the endovenous route. The main characteristics of vaptans are their effect on free water elimination without affecting electrolyte excretion. There are several studies on the effects of these drugs in hypervolemic hyponatremia (heart failure, hepatic cirrhosis) as well as in normovolemic hyponatremia (inappropriate secretion of ADH [SIADH]).
Current studies show that the vaptans are effective and well tolerated, although knowledge of these drugs remains limited. There are no studies of the use of vaptans in severe hyponatremia. Osmotic demyelination syndrome due to excessively rapid correction of hyponatremia has not been described.
Keywords:
Vasopressin
Hyponatremia
AVP receptor
Antagonist receptor
El Texto completo está disponible en PDF
Bibliografía
[1.]
G.L. Robertson, E.A. Mahr, S. Athar, T. Sinha.
Development and clinical application of a new method for the radioimmunoassay of arginine vasopressin in human plasma.
J Clin Invest, 52 (1973), pp. 2340-2352
[2.]
P. Gross, H. Pehrisch, W. Rascher, A. Schöming, E. Hackenthal, E. Ritz.
Pathogenesis of clinical hyponatremia. Observations of vasopressin and fluid intake in 1 000 hyponatremic medical patients.
Eur J Clin Invest, 17 (1987), pp. 123-129
[3.]
A. Leaf, A.R. Mamby.
An antidiuretic mechanism not regulated by extracelullar fluid tonicity.
J Clin Invest, 31 (1952), pp. 60-71
[4.]
R.W. Schrier, T. Berl.
Nonosmolar factors affecting renal water excretion.
N Engl J Med, 292 (1975), pp. 81-87
[5.]
R.W. Schrier.
Pathogenesis of sodium and water retention in high-output and low-output cardiac failure, nephrotic syndrome, cirrhosis, and pregnancy.
N Engl J Med, 319 (1988), pp. 1065-1072
[6.]
J. Boykin, A. De Torrente, G.L. Robertson, A. Erickson, R.W. Schrier.
Persistent plasma vasopressin levels in the hypoosmolar state associated with mineralcorticod deficiency.
Miner Elecrolyte Metab, 2 (1979), pp. 310-315
[7.]
D. Bichet, V. Szatawicz, C. Chaimovitz, R.W. Schrier.
Role of vasopressin in abnormal water excretion in cirrhotic patients.
Ann Intern Med, 96 (1982), pp. 413-417
[8.]
S.R. Goldsmith, G.S. Francis, A.W. Cowley.
Arginine vasopressin and the renal response to water loading in congestive heart failure.
Am J Cardiol, 58 (1986), pp. 295-299
[9.]
M. Usberti, S. Federico, S. Meccariello, B. Cianciaruso, M. Balleta, C. Pecovaro, et al.
Role of plasma vasopressin in the impairment of water excretion in nephrotic syndrome.
Kidney Int, 25 (1984), pp. 422-429
[10.]
R. Zerbe, L. Stropes, G. Robertson.
Vasopressin function in the syndrome of inappropiate antidiuresis.
Ann Rev Med, 31 (1980), pp. 315-327
[11.]
M. Manning, W.H. Sawyer.
Development of selective agonists and antagonists of vasopresin and oxytocin.
Vasopressin, pp. 131-144
[12.]
M. Manning, W.H. Sawyer.
Antagonists of vasopressin and oxytocin:current status and future perspectives.
Vasopresin, pp. 297-309
[13.]
Y. Yamamura, H. Ogawa, H. Yamashita, T. Chihara, H. Miyamoto, S. Nakamura, et al.
Characterization of a novel aquaretic agent OPC-31260 as an orally efective nonpeptide vasopressin V2 receptor antagonist.
Br J Pharmacol, 105 (1992), pp. 787-791
[14.]
A. Ohnishi, Y. Orita, R. Okahara, R. Fujihara, T. Inove, Y. Yamamura.
Potent aquaretic agent. A novel nonpeptide selective vasopressin 2 antagonist (OPC-31260) in men.
J Clin Invest, 92 (1993), pp. 2653-2659
[15.]
J.G. Verbalis, S.R. Goldsmith, A. Greenberg, R.W. Schrier, R.H. Sterns.
Hyponatremia treatment guidelines 2007: expert panel recommendations.
Am J Med, 120 (2007), pp. S1-S21
[16.]
G. Serradeil-Le Gal, J. Wagnon, G. Garcia, C. Lacour, P. Guinaudou, B. Christophe, et al.
Biochemical and pharmacological properties of SR 49059, a new potent non-peptide antagonist of rat and human vasopressin V1 receptors.
J Clin Invest, 92 (1993), pp. 224-231
[17.]
C. Serradeil-LeGal, C. Lacour, G. Valette, G. Garcia, L. Foulon, G. Galindo, et al.
Characterisation of SR 121 463A, a highly potent and selective, orally active vasopressin V2 receptor antagonist.
J Clin Invest, 98 (1996), pp. 2729-2738
[18.]
A. Matsuhisa, A. Tanaka, K. Kikuchi, Y. Shimada, T. Yatsu, W.A. Yanagisa.
Non peptide arginine vasopressin antagonists for both V1a and V2-receptors: synthesis and pharmacological properties of 2-phenyl4-(2,3,4,5-tetrahydro-1H-1-benzazepin-1-y)-Carbonyl) benzanilide derivations.
Chem Pharm Bull, 45 (1997), pp. 1870-1874
[19.]
A. Tahara, Y. Tomura, K. Wada, T. Kusayama, J. Tsukuda, M. Takanashi, et al.
Pharmacological profile of YM087, a novel potent nonpeptide vasopressin V1A and V2 receptor antagonist, in vitro and in vivo.
J Phamarcol Exp Ther, 282 (1997), pp. 301-308
[20.]
C. Serradeil-Le Gal, J. Wagnon, J. Simiand, G. Griebel, C. Lacour, G. Guillon, et al.
Characterization of SSR149415, a selective and orally-active vasopressin V1b receptor antagonist.
J Pharmacol Exp Ther, 300 (2002), pp. 1122-1130
[21.]
D. Bolignano, G. Coppolino, M. Criseo, S. Campo, A. Romeo, M. Buemi.
Aquaretic agents: What's beyond the treatment of hyponatremia?.
Curr Pharmaceut Desig, 13 (2007), pp. 865-871
[22.]
D.G. Bichet.
Vasopressin receptors in health and disease.
Kidney Int, 49 (1996), pp. 1706-1711
[23.]
C.L. Holmes, D.W. Landry, J.T. Granton.
Science review: vasopressin and the cardiovascular system part 1-receptor physiology.
Crit Care, 7 (2003), pp. 427-434
[24.]
L. Bankir.
Antidiuretic action of vasopressin: quantitative aspects and interaction between V1a and V2-receptor-mediated effects.
Cardiosvasc Res, 51 (2001), pp. 372-390
[25.]
M.A. Knepper, J.D. Wade, J. Terris, A. Ecelbarger, D. Marples, B. Mandon, et al.
Renal aquaporins.
Kidney Int, 49 (1996), pp. 1712-1717
[26.]
S. Nielsen, D. Marples, J. Frokiaer, M. Knepper, P. Agre.
The aquaporin family of water channels in kidney: an update on physiology and pathophysiology of aquaporin-2.
Kidney Int, 49 (1996), pp. 1718-1723
[27.]
S. Nielsen, T. Kwon, M. Christensen, D. Promeneur, J. Frokiaer, D. Marples.
Physiology and pahtophysiology of renal aquaporins.
J Am Soc Nephrol, 10 (1999), pp. 647-663
[28.]
S. Nielsen, J. Frokiaer, D. Marples, T. Kwon, P. Agre, M.A. Knepper.
Aquaporins in the kidney: from molecules to medicine.
Phsiol Rev, 82 (2002), pp. 205-244
[29.]
M. Buemi, F. Corica, G. Di Pasquale, C. Aloisi, M. Sofi, G. Latassa, et al.
Water immersion increases urinary excretion of aquaporin-2 in healthy humans.
Nephron, 85 (2000), pp. 20-26
[30.]
PE. Pool.
The clinical significance of neurohormonal activation.
Clin Ther, 19 (1997), pp. 53-73
[31.]
M. Thibonnier.
Vasopressin receptor antagonists in heart failure.
Curr Opin Pharmacol, 3 (2003), pp. 683-687
[32.]
C.R. Lee, M.L. Watkins, J.H. Patterson, W. Gattis, C.M. O’ Connor, M. Gheorghiade, et al.
Vasopressin: a new target for the treatment of heart failure.
Am Heart J, 146 (2003), pp. 9-18
[33.]
S.R. Goldsmith.
The role of vasopressin in congestive heart failure.
Clev Clin J Med, 73 (2006), pp. S19-S23
[35.]
A. Greenberg, J.G. Verbalis.
Vasopressin receptor antagonists.
Kidney Int, 69 (2006), pp. 2124-2130
[36.]
C. Palm, F. Pistroch, K. Herbrig, P. Gross.
Vasopressin as aquaretic agents for the treatment of hyponatremia.
Am J Med, 119 (2006), pp. S87-S92
[37.]
F. Quittnat, P. Gross.
Vaptans and the treatment of water-retaining disorders.
Semin Nephrol, 26 (2006), pp. 234-243
[38.]
R. Macion-Dazard, N. Callahan, Z. Xu, N. Wu, M. Thibonnier, M. Sholam.
Mapping the binding site of six nonpeptide antagonists to the human V2-renal vasopressin receptor.
J Pharmacol Exp Ther, 316 (2006), pp. 564-571
[39.]
F. Ali, M. Guglin, P. Vaitkevicius, J.K. Ghali.
Therapeutical potential of vasopressin receptor antagonists.
Drugs, 67 (2007), pp. 847-858
[40.]
G. Decaux, A. Soupart, G. Vassart.
Non-peptide arginine-vasopressin antagonists: the vaptans.
Lancet, 371 (2008), pp. 1624-1632
[41.]
P.S. Chan, J. Coupet, H.C. Park, F. Lai, D. Hartupee, P. Cervoni, et al.
VPA-985 a nonpeptide oraly active and selective vasopressin V2 receptor antagonist.
Vasopressin and oxytocin; molecular, cellular and clinical advances, pp. 439-443
[42.]
F. Wong, A.T. Blei, L.M. Biendis, P.J. Thuluvath.
A vasopressin receptor antagonist (VPA-985) improves serum sodium concentration in patients with hyponatremia: a multicenter, randomized, placebo-controlled trial.
Hepatology, 37 (2003), pp. 182-191
[43.]
A.L. Gerbes, V. Gulberg, P. Gines, G. Decaux, P. Gross, H. Gandjini, et al.
Therapy of hyponatremia in cirrhosis with a vasopressin receptor antagonist: a randomized double-blind multicenter trial.
Gastroenterology, 124 (2003), pp. 933-939
[44.]
W.T. Abraham, A.A. Shamshirsaz, K. McFann, R.M. Oren, R.W. Schrier.
Aquaretic effect of lixivaptan, an oral, non-peptide, selective V2 receptor vasopressin antagonist, in New York Heart Association Functional Class II and III Chronic Heart Failure Patients.
J Am Coll Card, 47 (2006), pp. 1615-1621
[45.]
A. Soupart, P. Gross, J.J. Legros, S. Alföldi, S. Annane, H. Heshmati, et al.
Successful long-term treatment of hyponatremia in syndrome of inappropiate antidiuretic hormone secretion with satavaptan (SR 121 463 B), an orally active non peptide vasopressin V2-receptor antagonist.
Clin J Am Soc Nephrol, 1 (2006), pp. 1154-1160
[46.]
Long-term efficacy of satavaptan in patients with SIADH-related hyponatremia (editorial).
Nat Clin Pract, 3 (2007), pp. 122
[47.]
Y. Yamamura, S. Nakamura, S. Itoh, T. Hirano, T. Onogawa, T. Yamashita, et al.
OPC 41061, a highly potent human vasopressin V2 receptor antagonist: pharmacological profile and aquaretic effect by single and multple oral dosing in rats.
J Pharmacol Exp Ther, 287 (1998), pp. 860-867
[48.]
J.G. Verbalis.
AVP receptor antagonists as aquaretics: review and assessment of clinical data.
Clev Clin J Med, 73 (2006), pp. S24-S33
[49.]
J.E. Udelson, C. Orlalindi, T. O’Brien, et al.
Vasopressin receptor blockade in patients with congestive heart failure: results from a placebo-controlled, randomized study comparing the effects of tolvaptan, furosemide, and their combination (abstract).
J Am Coll Cardiol, 39 (2002), pp. 156A
[50.]
J.E. Uldeson.
The METEOR Trial Investigators Multicenter randomized double-blind, placebo-controlled, efficacy study on the effects of oral tolvaptan on LV dilatation and function in patients with HF and LV systolic dysfunction.
The 9th Annual Scientfic Meeting of Heart Failure Society of America,
[51.]
J.E. Udelson, F.A. McGrew, E. Flores, H. Ibrahim, S. Katz, G. Koshkarian, et al.
Multicenter, randomized, double-blind, placebo study on the effect of oral tolvaptan on left ventricular dilation and function inpatient with heat failure and systolic dysfunction.
J Am Coll Cardiol, 49 (2007), pp. 2151-2159
[52.]
R.W. Schrier, P. Gross, M. Gheorgiade, et al.
Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia.
N Engl J Med, 355 (2006), pp. 2099-2112
[53.]
W.L. Weise, J.M. Rimmer, V.L. Hood.
Tolvaptan for hyponatremia (letter).
N Engl J Med, 356 (2007), pp. 961
[54.]
R.M. Hays.
Vasopressin antagonists-Progress and Promise.
N Engl J Med, 355 (2006), pp. 2146-2148
[55.]
S.M. Adler, J.G. Verbalis, J. Ouyang, et al.
Management of SIADH with tolvaptan: a subanalysis from the SALT trials.
American Association of Clinical Endocrinologists Conference,
[56.]
G. Decaux.
Long-term treatment of patients with inappropiate secretion of antidiuretic hormone by the vasopressin antagonist conivaptan, urea, or furosemide.
Am J Med, 110 (2001), pp. 582-584
[57.]
J.K. Ghali, M.J. Koren, J.R. Taylor, E. Brooks-Asplund, K. Fan, W.A. Long, et al.
Efficacy and safety of oral conivaptan: a V1A/V2 vasopressin receptor antagonist, assesssed in a randomized, placebo-controlled trial in patients with euvolemic or hypervolemic hyponatremia.
J Clin Endocrinol Metab, 91 (2006), pp. 2145-2152
[58.]
J.E. Udelson, W.B. Smith, G.H. Hendrix, C.A. Painchaud, M. Ghazzi, I. Thomas, et al.
Acute hemodynamic effects of conivaptan, a dual V(1A) and V(2) vasopressin recetor antagonist, in patients with advanced heart failure.
Circulation, 104 (2001), pp. 2417-2423
[59.]
D. Zeltser, S. Rosanasky, H. Van Rensburg, J.G. Verbalis, N. Smith.
Assessment of the efficacy and safety of intravenous conivaptan in euvolemic and hypervolemic hyponatremia.
Am J Nephrol, 27 (2007), pp. 447-457
[60.]
J.G. Verbalis, D. Zeltser, N. Smith, A. Barve, M. Andoh.
Assessment of the efficacy and safety of intravenous conivaptan in patients with euvolemic hyponatraemia: subgroup analysis of a randomized, controlled study.
Clin Endocrinol (Oxf), 69 (2008), pp. 159-168
[61.]
T. Murphy, R. Dhar, M. Diringer.
Conivaptan bolus dosing for the correction of hyponatremia in the neurointensive care unit.
Neurocrit Care, (2009),
[62.]
W.L. Wright, W.H. Asbury, J.L. Gilmore, O.B. Samuels.
Conivaptan for hyponatremia in the neurocritical care unit.
Neurocrit Care, (2008),
[63.]
J.D. Fields, A. Bhardwaj.
Non-peptide arginine-vasopressin antagonists (vaptans) for the treatment of hyponatremia in neurocritical care: a new alternative?.
Neurocrit Care, 1 (2009), pp. 1-4
[64.]
D. Hayoz, G. Bizzini, B. Noel, M. Depairon, C. Burnier, A. Faveau, et al.
Effect of SR49059, a V1a vasopressin receptor antagonist in Raynaud's phenomenon.
Rheumatology, 39 (2000), pp. 1132-1138
[65.]
M. Steinwall, T. Bossmar, R. Brouard, T. Laudanski, P. Olofsson, R. Urban, et al.
The effect of Relcovaptan (SR 49059), an orally active vasopressin V1a-receptor anatagonist on uterine contraction in preterm labor.
Gynecol Endocrinol, 20 (2005), pp. 104-109
[66.]
R. Brouard, T. Bossmar, D. Fournie-Lloret, D. Chassard, M. Akerlund.
Effect of SR 49059, and orally active V1a vasopressin receptor antagonist in the prevention of dysmenorrhoea.
Br J Obstet Gynaecol, 106 (1999), pp. 1047-1053
[67.]
H. Daidoh, H. Morita, J. Hanafusa, T. Mune, H. Murase, M. Sato, et al.
In vivo and in vitro effects of AVP and V1a receptor antagonist on Cushing's syndrome due to ACTH-independent bilateral macronodular adrenocortical hyperplasia.
Clin Endocrinol (Oxf), 49 (1998), pp. 403-409
[68.]
N. Sonino, M. Boscaro, F. Fallo.
Pharmacologic management of Cushing syndrome: new target for therapy.
Treat Endocrinol, 4 (2005), pp. 87-94
[69.]
G. Griebel, J. Simiand, C. Serradeil-Le Gal, J. Wagnon, M. Pascal, B. Scatton, et al.
Anxiolytic-and-antidepressant-like effects of the non-peptide vasopressin V1b-receptor antagonist. SSR149415, suggest and innovatrice approach for the treatment of stress-related disorders.
PNAS, 99 (2002), pp. 6370-6375
[70.]
P. Gross.
Treatment of hyponatremia.
Inter Med, 47 (2008), pp. 885-891
[71.]
G. Decaux, A. Soupart.
Treatment of symptomatic hyponatremia.
Am J Med Sci, 326 (2003), pp. 25-30
[72.]
R.H. Sterns, S.U. Nigwekar, J.K. Hix.
The treatment of hyponatremia.
Semin Nephrol, 29 (2009), pp. 282-299
[73.]
Y.H. Lien, J.I. Shapiro.
Hyponatremia: clinical diagnosis and management.
Am J Med, 120 (2007), pp. 653-658
[74.]
K.P. Goh.
Management of hyponatremia.
Am Fam Phys, 69 (2004), pp. 2387-2394
[75.]
R. Abbott, E. Silber, J. Felber, E. Ekpo.
Osmotic demyelination syndrome.
Br Med J, 331 (2005), pp. 829-830
[76.]
H.J. Adrogué.
Consequences of inadequate management of hyponatremia.
Am J Nephrol, 25 (2005), pp. 240-249
[77.]
H. Furst, K. Hallows, J. Post, S. Chen, W. Kotzker, S. Goldfarb, et al.
The urine/plasma electrolyte ratio: a predictive guide to water restricion.
Am J Med Sci, 319 (2000), pp. 240-244
[78.]
M.G. White, C.D. Fetner.
Treatment of the syndrome of inappropiate secretion of antiduretic hormone with lithium carbonate.
N Engl J Med, 292 (1975), pp. 81-87
[79.]
D.N. Juurlink, M.M. Mamdani, A. Kopp, P.A. Rochon, K.I. Shulman, D.A. Redelmeier.
Drug-induced lithium toxicity in the elderly: a population-based study.
J Am Geriatr Soc, 52 (2004), pp. 794-798
[80.]
J.N. Forrest Jr, M. Cox, C. Hong, G. Morrison, M. Bia, I. Singer.
Superiority of demeclocycline over lithium in the treatment of chronic syndrome of inappropiate secretion of antidureitc hormone.
N Engl J Med, 298 (1978), pp. 178-179
[81.]
G. Decaux, S. Brimioulle, F. Genette, Jl. Mockel.
Treatment of the syndrome of inappropiate secretion of antidureitc hormone by urea.
Am J Med, 69 (1980), pp. 99-106
[82.]
G. Decaux, S. Brimioulle, F. Genette, J. Mockel.
Treatment of the syndrome of inappropiate secretion of antiduretic hormone by urea.
Am J Med, 83 (1981), pp. 1081-1083
[83.]
D. Hantman, B. Rossier, R. Zohlman, R. Schrier.
Rapid correction of hyponatremia in the syndrome of inappropiate secretion of antiduretic hormone. An alternative treatment to hypertonic saline.
Ann Intern Ned, 78 (1973), pp. 870-876
[84.]
R.W. Lehrich, A. Greenberg.
When is it appropiate to use vasopressin receptor antagonists?.
J Am Soc Nephrol, 19 (2008), pp. 1054-1058
[85.]
A. Rai, A. Ehaley-Connell, N.E. McFarla, J.R. Sowers.
Hyponatremia, arginine vasopressin dysregulation, and vasopressin receptor antagonism.
Am J Nephrol, 26 (2006), pp. 579-589
[86.]
K.E. Yeates, A.R. Moreton.
Vasopressin antagonists: role in the management of hyponatremia.
Am J Nephrol, 26 (2006), pp. 348-355
[87.]
E.J. Hoorn, R. Zietse.
Hyponatremia revisited: translating physiology to practice.
Nephron Physiol, 108 (2008), pp. 46-59
[88.]
D.L. Jennings, J.S. Kalus.
Tolvaptan.
Formulary, 43 (2008), pp. 236-249
[89.]
J.K. Ghali, B. Hamad, U. Yasothan, P. Kirkpatrick.
Tolvaptan.
Nat Rev, 8 (2009), pp. 611-612
[90.]
P. Gross, T. Marczewski, K. Herbrig.
The vaptans ante portas: a status report.
Nephrol Dial Transplant, 24 (2009), pp. 1371-1373
[91.]
B.J. Feldman, S.M. Rosenthal, G.A. Vargas, R.G. Fenwick, E.A. Huang, M. Matsuda-Abedini, et al.
Nephrogenic syndrome of inappropiate antidiuresis.
N Engl J Med, 352 (2005), pp. 1884-1890
[92.]
G. Decaux, F. Vandergheynst, Y. Bouko, J. Parma, G. Vassart, C. Vilain.
Nephrogenic syndrome of inappropiate antiduresis in adults: high phenotypic variability in men and women from a large pedigree.
J Am Soc Nephrol, 18 (2007), pp. 606-612
[93.]
G. Decaux.
The syndrome of inappropiate secretion of antidiuretic hormone (SIADH).
Semin Nephrol, 29 (2009), pp. 239-256
[94.]
P.H. Baylis.
The syndrome of inappropiate antidiuretic hormone secretion.
Int J Biochem Cell Biol, 35 (2003), pp. 1495-1499
[95.]
D.H. Ellison, T. Berl.
The syndrome of inappropiate antidiuresis.
N Engl J Med, 356 (2007), pp. 2064-2072
[96.]
M.J. Halperin, K.S. Kamel.
A new look at an old problem: therapy of chronic hyponatremia.
Nat Clin Pract Nephrol, 3 (2007), pp. 2-3
[97.]
G. Fernández-Varo, J. Ros, P. Cejudo-Martín, C. Cano, V. Arroyo, F. Rivera, et al.
Effect of the V1a/V2-AVP receptor antagonist. Conivaptan, on renal water metabolism and systemic hemodynamics in rats with cirrhosis and ascitis.
J Hepatol, 38 (2003), pp. 755-761
[98.]
S.R. Goldsmith.
Is there a cardiovascular rationale for the use of combined vasopressin V1a/V2 receptor antagonists?.
Am J Med, 119 (2006), pp. S93-S96
[99.]
S.R. Goldsmith.
Treatment options for hyponatremia in heart failure.
Heart Fail Rev, 14 (2009), pp. 65-73
[100.]
X. Wang, C.J. Ward, P.C. Harris, V.E. Torres.
Cyclic nucleotide signaling in plycystic kidney disease.
Kidney Int, (2009),
[101.]
V.E. Torres, P.C. Harris.
Autosomal dominant polycystics kidney disease: the last 3 years.
Kidney Int, 76 (2009), pp. 149-158
[102.]
V.E. Torres.
Vasopressin in chronic disease: an elephant in the room?.
Kidney Int, 76 (2009), pp. 925-928
[103.]
V.E. Torres.
Vasopressin in polycystic kidney disease.
Kidney Int, 68 (2005), pp. 2405-2418
Copyright © 2010. Sociedad Española de Endocrinología y Nutrición