Document Detail


Plasma vasopressin and V2 receptor in the endolymphatic sac in patients with delayed endolymphatic hydrops.
MedLine Citation:
PMID:  19638944     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: There are some kinds of sicknesses provoked by inadequate adaptation to physical and/or psychogenic stress in daily life. Delayed endolymphatic hydrops (DEH) is an inner ear disease like Ménière's disease (MD) characterized by episodic vertigo in the setting of preexisting unilateral deafness that especially occurs in civilized people with a stressful lifestyle. Its otopathologic finding was demonstrated to be inner ear endolymphatic hydrops through a temporal bone study in 1976, as in the case with MD in 1938. To elucidate the relationship between stress and the inner ear, we examined the plasma antidiuretic stress hormone vasopressin (pAVP) and its type 2 receptor (V2R) expression in the endolymphatic sac in patients with DEH. STUDY DESIGN: A prospective molecular biological study. METHODS: Between 1998 and 2007, we enrolled 20 patients with ipsilateral DEH to examine their pAVP during remission from vertigo attacks. Plasma vasopressin was also examined in 87 patients with unilateral MD and 30 control patients with chronic otitis media. Using the real-time polymerase chain reaction method with tissue samples obtained during surgery, we examined V2R mRNA expression in the endolymphatic sac in 6 patients with ipsilateral DEH, 9 patients with unilateral MD, and 6 control patients with acoustic neuroma. RESULTS: Plasma vasopressin (1.5 times versus controls; unpaired t test, p = 0.140) and V2R mRNA expression in the endolymphatic sac (35.8 times versus controls; unpaired t test, p = 0.002) were higher in patients with DEH compared with those with acoustic neuroma. There were no significant differences in pAVP or V2R expression in the endolymphatic sac between DEH and MD. Patients with DEH showed a significantly negative correlation between pAVP and V2R (Pearson test, r = -0.92, p = 0.009) as in those with MD (Pearson test, r = -0.68, p = 0.043). CONCLUSION: Civilized people are frequently exposed to stress in their daily life, and pAVP can easily become elevated at any time. Therefore, a negative feedback system between pAVP and V2R in the endolymphatic sac may function for inner ear fluid homeostasis against stress-induced increases in pAVP. For the pathogenesis of endolymphatic hydrops resulting in vertigo attacks in patients with DEH as well as MD, pAVP may represent a matter of consequence, but V2R overexpression in the endolymphatic sac could be much more essential as a basis for these diseases.
Authors:
Tadashi Kitahara; Chie Maekawa; Kaoru Kizawa; Arata Horii; Katsumi Doi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology     Volume:  30     ISSN:  1537-4505     ISO Abbreviation:  Otol. Neurotol.     Publication Date:  2009 Sep 
Date Detail:
Created Date:  2009-08-25     Completed Date:  2009-11-16     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100961504     Medline TA:  Otol Neurotol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  812-9     Citation Subset:  IM    
Affiliation:
Department of Otolaryngology, Osaka University, School of Medicine, Suita-city, Osaka, Japan. tkitahara@ent.med.osaka-u.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Adult
Blotting, Western
Data Interpretation, Statistical
Endolymphatic Hydrops / diagnosis,  genetics*,  metabolism*
Endolymphatic Sac / metabolism*
Female
Humans
Male
Meniere Disease / complications
Middle Aged
Otologic Surgical Procedures
Prospective Studies
RNA / biosynthesis,  genetics
Receptors, Vasopressin / genetics,  metabolism*
Reverse Transcriptase Polymerase Chain Reaction
Vasopressins / blood*
Vertigo / etiology
Chemical
Reg. No./Substance:
0/Receptors, Vasopressin; 11000-17-2/Vasopressins; 63231-63-0/RNA

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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