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Cited by 300Ion Transport and Channel RegulationElectrolyte and hormonal disordersCardiovascular, Neuropeptides, and Oxidative Stress Research

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Antidiuretic action of vasopressin: quantitative aspects and interaction between V1a and V2 receptor-mediated effects

Bankir, L·2001·Cardiovascular Research
DOI 10.1016/s0008-6363(01)00328-5
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Abstract

(1) Vasopressin (VP), or antidiuretic hormone, is secreted in response to either increases in plasma osmolality (very sensitive stimulus) or to decreases in plasma volume (less sensitive stimulus). Its normal plasma level is very low (about 1 pg/ml, i.e. 10(-12) M), close to the detection limit of present immunoassays, and distinct antidiuretic effects are observed after infusion of small undetectable amounts of VP. (2) This antidiuretic action results from three main effects of VP on principal cells of the collecting duct (CD) mediated by occupancy of peritubular V2 receptors. (i) Increase in water permeability along the entire CD (via AQP2). (ii) Increase in urea permeability in only the terminal inner medullary CD (via UT-A1). (iii) Stimulation of sodium reabsorption, mainly in the cortical and outer medullary CD (via ENaC). VP also acts on medullary vasculature (V1a receptors) to reduce blood flow to inner medulla without affecting blood flow to outer medulla. Besides these actions, all concurring to increase urine osmolality in different and additive ways, other VP effects, probably exerted through V1a receptors located on luminal membrane, tend to limit the antidiuretic effects of the hormone. They induce the formation of prostaglandins which reduce V2-dependent cAMP accumulation in these cells and thus partially inhibit all three V2 effects. (3) Because urine is first diluted along the nephron before being concentrated in the medulla, VP is required, not only for urine concentration, but first for re-equilibration of tubular fluid osmolality with plasma osmolality, a step taking place in the renal cortex, and achieved through the reabsorption of large quantities of water (more than what is subsequently reabsorbed in the medulla to concentrate urine). Accordingly, VP effects on urine flow-rate are not linear. Small changes in plasma VP in the low range of urine osmolality will induce wide changes in urinary flow-rate, whereas in the upper range of urine osmolality larger changes in plasma VP induce much more limited further reduction in urine flow-rate. (4) Most likely, the different effects of VP require different levels of VP concentration to occur and are thus recruited successively with progressive rise in VP secretion.

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Research works printed but not linked: 26

  1. Brattleboro rats. Am J Physiol 1984;246:F819-F827.
  2. editor, Handbook of physiology, New York: Oxford University
  3. Okada H, Suzuki H, Kanno Y, Yamamura Y, Saruta T. Effects of excretion of water loads. Regul Pept 1993;45:217-223. vasopressin V1 and V2 receptor antagonists on progressive renal
  4. Shimizu K, Nakao A, Nonaka T, Oka H. Identification of vas- Ther 1995;272:546-551. opressin and determination of its corticomedullary levels in rat
  5. Burnier M, Fricker AF, Hayoz D, Nussberger J, Brunner HR. kidney tissue. Kidney Int 1984;26:785-790. Pharmacokinetic and pharmacodynamic effects of YM087, a com-
  6. Kamoi K, Ebe T, Kobayashi O et al. Atrial natriuretic peptide in 1988;295:314-319. patients with the syndrome of inappropriate antidiuretic hormone
  7. Share L, Wang YX, Crofton JT. Gender differences in the actions of secretion and with diabetes insipidus. J Clin Endocrinol Metab vasopressin. In: Saito T, Kurokawa K, Yoshida S, editors, Neuro- 1990;70:1385-1390. hypophysis: recent progress of vasopressin and oxytocin research,
  8. Wang YX, Crofton JT, Liu H, Brooks DP, Share L. Effects of Ther 1990;255:264-270. ¨gonadectomy on sexually dimorphic antidiuretic action of vas-
  9. Choukroun G, Schmitt F, Martinez F, Drueke T, Bankir L. Low opressin in conscious rats. Am J Physiol 1994;267:R536-R541. urine flow-rate reduces the capacity to excrete a sodium load in man. Am J Physiol 1997;273:R1726-R1733.
  10. Nicco C, Wittner M, DiStefano A, Jounies S, Bankir L, Bouby N. rats: role of prostaglandins. Am J Physiol 1993;264:F629-F636. Chronic exposure to vasopressin upregulates ENaC and sodium transport in the rat collecting duct. Hypertension 2001; in press.
  11. Bankir L, Bouby N, Trinh-Trang-Tan MM, Ahloulay M, Promeneur normal human subjects. J Lab Clin Med 1991;117:51-59.
  12. Martin H, Bankir L. Differences in renal function between Wistar 21 and Sprague-Dawley rats. J Am Soc Nephrol 1995;6:1023, Ab-
  13. Park CH, Lock TYW, Tanikella TK et al. VNA-932, a nonpeptide V2 selective vasopressin agonist. J Am Soc Nephrol 1999;10:22A,
  14. Am J Physiol 1987;253:F823-F832.
  15. BM, editor, The kidney, 6th ed., Philadelphia: W.B. Saunders, 2000, 2000;168:239-244. pp. 637-679.
  16. Masilamani S, Knepper MA, Burg MB. Urine concentration and 1985;249:R643-R666. dilution. In: Brenner BM, editor, The kidney, 6th ed., Philadelphia:
  17. Tomita K, Pisano JJ, Knepper M. Control of sodium and potassium 1989;3:249-311. transport in the cortical collecting duct of the rat. J Clin Invest
  18. Harmanci MC, Stern P, Kachadorian WA, Valtin H, DiScala VA. 1985;76:132-136. Vasopressin and collecting duct intramembranous particle clusters, a
  19. Star RA, Nonoguchi H, Balaban R, Knepper MA. Calcium and 1 membrane Na -conductance. Pflugers Arch 1987;409:81-92. cyclic adenosine monophosphate as second messengers for vas- 1
  20. Wang WH, Giebisch G. Dual modulation of renal ATP-sensitive 1996;17:477-481.
  21. Rouffignac-de C, Elalouf JM. Effects of calcitonin on the renal 1977;12:313-323.
  22. concentrating mechanism. Am J Physiol 1983;245:F506-F511.
  23. Wittner M, DiStefano A, Wangemann P et al. Differential effects of Clin Invest 1966;45:337-345.
  24. Bouby N, Ahloulay M, Nsegbe E, Dechaux M, Schmitt F, Bankir 1997;51:381-385.
  25. Bankir L, Ahloulay M, Bouby N, Machet F, Trinh-Trang-Tan MM. tidiuretic action. J Am Soc Nephrol 1996;7:842-851. Direct and indirect effects of vasopressin on renal hemodynamics.
  26. Bankir L, Martin H, Bouby N. Vasopressin increases GFR in rats. In: Gross P, Richter D, Robertson GL, editors, Vasopressin, Paris: Disclosure of this effect was previously obscured by inadequate John Libbey Eurotext, 1993, pp. 393-406. experimental protocols. FASEB J 1998;12:A331, Abstract.

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Metadata

Authors
Bankir, L.
Affiliations
Inserm (FR)
Corresponding author
Bankir, L
ORCID
Bankir, L
Venue
Cardiovascular Research
Publisher
Oxford University Press (OUP)
Published
2001-08-15
Volume
51
Issue
3
Pages
372-390
ISSN
0008-6363 (ISSN-L)
DOI
10.1016/s0008-6363(01)00328-5
OpenAlex
W1991465398
Cited by
300
References
126
Citations by year
2026: 2 · 2025: 11 · 2024: 6 · 2023: 11 · 2022: 10 · 2021: 10 · 2020: 15 · 2019: 10 · 2018: 9 · 2017: 9 · 2016: 14 · 2015: 14 · 2014: 20 · 2013: 18 · 2012: 19
FWCI
0.47
Type
journal article
Language
en
Open access
closed
Locations
  • Cardiovascular Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
Danone
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
  • Health Sciences › Medicine › Nephrology › Electrolyte and hormonal disorders
  • Health Sciences › Medicine › Surgery › Cardiovascular, Neuropeptides, and Oxidative Stress Research
Keywords
vasopressin, V1a receptor, V2 receptor, collecting duct, principal cells, water permeability, aquaporin-2, urea permeability, UT-A1, epithelial sodium channel, sodium reabsorption, medullary blood flow, prostaglandins, cyclic AMP, urine osmolality, urinary flow rate, plasma osmolality, plasma volume, hormone dose-response
MeSH terms
Diuresis, Humans, Kidney, Liver, Respiratory System, Vasopressins, Receptors, Vasopressin

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