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Abstract <p>Vasopressin (antidiuretic hormone, ADH) plays an importantrole in the regulation of water–salt balance in mammals. Brattlebororats lack endogenous ADH due to a mutation in the ADH-neurophysin gene,leading to a recessive form of central diabetes insipidus. Thiswork investigated the role of cAMP in ADH-dependent regulation ofwater permeability of the apical and basolateral membranes in outermedullary collecting duct (OMCD) principal cells in Brattlebororats. Data obtained from water-loaded Wistar rats were used as acontrol. The osmotic water permeability coefficient (<i>P</i> <sub><i>f</i></sub>)of principal cells in isolated OMCD was assessed using a methodbased on calcein fluorescence quenching by cytoplasmic proteins.The content of aquaporins AQP2 and AQP3 in the membrane fractionof outer medullary cells was evaluated by Western blotting. Boththe vasopressin V2 receptor agonist (DDAVP, 10<sup>–8</sup> M)and the cell-permeable cAMP analog (DB-cAMP, 10<sup>–5</sup> M)significantly increased the water permeability of both the apicaland basolateral membranes of OMCD principal cells in both rat strainsafter a 25-min exposure, with the cAMP analog having a more pronouncedeffect compared to DDAVP. We have previously shown that short-termexposure to DDAVP increased AQP2 content in the membrane fraction ofWistar rats and AQP2-3 content in Brattleboro rats. In this study,Western blotting demonstrated that DB-cAMP increased the contentof AQP2, but not AQP3, in the membrane fraction of the renal outermedulla in both Wistar and Brattleboro rats. It can be assumed thatin Brattleboro rats, AQP3-mediated water transport across the basolateral membraneof OMCD principal cells is regulated by ADH not only through a cAMP-dependentpathway but also with the involvement of other, including calcium-related,secondary messenger systems.</p>

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Vasopressin-Dependent Water Permeability Regulation in Collecting Duct Principal Cells of Brattleboro Rats: the Role of cAMP

  • 期刊论文

  • 发表日期：

    2025年12月19日

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  • G. S. Baturina,
  • L. E. Katkova,
  • E. I. Solenov

摘要

Abstract

Vasopressin (antidiuretic hormone, ADH) plays an importantrole in the regulation of water–salt balance in mammals. Brattlebororats lack endogenous ADH due to a mutation in the ADH-neurophysin gene,leading to a recessive form of central diabetes insipidus. Thiswork investigated the role of cAMP in ADH-dependent regulation ofwater permeability of the apical and basolateral membranes in outermedullary collecting duct (OMCD) principal cells in Brattlebororats. Data obtained from water-loaded Wistar rats were used as acontrol. The osmotic water permeability coefficient (P f)of principal cells in isolated OMCD was assessed using a methodbased on calcein fluorescence quenching by cytoplasmic proteins.The content of aquaporins AQP2 and AQP3 in the membrane fractionof outer medullary cells was evaluated by Western blotting. Boththe vasopressin V2 receptor agonist (DDAVP, 10–8 M)and the cell-permeable cAMP analog (DB-cAMP, 10–5 M)significantly increased the water permeability of both the apicaland basolateral membranes of OMCD principal cells in both rat strainsafter a 25-min exposure, with the cAMP analog having a more pronouncedeffect compared to DDAVP. We have previously shown that short-termexposure to DDAVP increased AQP2 content in the membrane fraction ofWistar rats and AQP2-3 content in Brattleboro rats. In this study,Western blotting demonstrated that DB-cAMP increased the contentof AQP2, but not AQP3, in the membrane fraction of the renal outermedulla in both Wistar and Brattleboro rats. It can be assumed thatin Brattleboro rats, AQP3-mediated water transport across the basolateral membraneof OMCD principal cells is regulated by ADH not only through a cAMP-dependentpathway but also with the involvement of other, including calcium-related,secondary messenger systems.