Vasopressin increases intracellular NO concentration via Ca2+ signaling in inner medullary collecting duct

Takefumi Mori, Jeffrey G. Dickhout, Allen W. Cowley

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)

Abstract

The present study was designed to determine whether arginine vasopressin (AVP) stimulates NO production in the epithelial collecting duct cells of the inner medulla (IMCDs) and if this is mediated through Ca2+ signaling. Thin tissue layers containing IMCDs were dissected from Sprague-Dawley rats. Intracellular Ca2+ concentration ([Ca2+]i) and NO production were measured in IMCDs by a fluorescence imaging system with the use of fura 2-AM and the cell-permeable form of the NO-sensitive dye 4,5-diaminofluorescein (DAF-2), respectively. AVP (100 nmol/L) produced a rapid peak increase in [Ca2+]i of 320±70 nmol/L within a few seconds and a sustained increase of 120+62 nmol/L. The peak increase in [Ca2+]i was followed by a significant increase of NO production (34±7 U). This was similar to that produced by 20/μmol/L of the NO donor DETA-NONOate (42±11 U). The NO scavenger carboxy-PTIO (100 μmol/L) or depletion of [Ca2+]i by preincubation with 5 μmol/L of the Ca2+-ATPase inhibitor thapsigargin in Ca2+-free buffer abolished the NO response to AVP. We conclude that AVP mobilizes Ca2+ to produce NO in IMCDs.

Original languageEnglish
Pages (from-to)465-469
Number of pages5
JournalHypertension
Volume39
Issue number2 II
DOIs
Publication statusPublished - 2002

Keywords

  • Calcium
  • Kidney
  • Nitric oxide
  • Signal transduction
  • Vasopressins

ASJC Scopus subject areas

  • Internal Medicine

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