Vasopressin increases intracellular NO concentration via Ca(2+) signaling in inner medullary collecting duct. Hypertension 2002 Feb;39(2 Pt 2):465-9
Date
03/08/2002Pubmed ID
11882591DOI
10.1161/hy02t2.102908Scopus ID
2-s2.0-0036175379 (requires institutional sign-in at Scopus site) 29 CitationsAbstract
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 Ca(2+) signaling. Thin tissue layers containing IMCDs were dissected from Sprague-Dawley rats. Intracellular Ca(2+) concentration ([Ca(2+)](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 [Ca(2+)](i) of 320 +/- 70 nmol/L within a few seconds and a sustained increase of 120 +/- 62 nmol/L. The peak increase in [Ca(2+)](i) was followed by a significant increase of NO production (34 +/- 7 U). This was similar to that produced by 20 micromol/L of the NO donor DETA-NONOate (42 +/- 11 U). The NO scavenger carboxy-PTIO (100 micromol/L) or depletion of [Ca(2+)](i) by preincubation with 5 micromol/L of the Ca(2+)-ATPase inhibitor thapsigargin in Ca(2+)-free buffer abolished the NO response to AVP. We conclude that AVP mobilizes Ca(2+) to produce NO in IMCDs.
Author List
Mori T, Dickhout JG, Cowley AW JrAuthor
Allen W. Cowley Jr PhD Professor in the Physiology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsArginine Vasopressin
Benzoates
Calcium
Drug Interactions
Imidazoles
In Vitro Techniques
Kidney Medulla
Male
Nitric Oxide
Rats
Rats, Sprague-Dawley
Signal Transduction
Time Factors