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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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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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