Premium
Specific changes in TRPV4 expression in the vasopressinergic cells in supraoptic nucleus of the rat brain following bile duct ligation (BDL) induced cirrhosis
Author(s) -
Carreño Flávia Regina,
Ji Lisa,
Cunningham J Thomas
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.967.10
Subject(s) - vasopressin , supraoptic nucleus , medicine , endocrinology , hyponatremia , hypothalamus
Inappropriate vasopressin (AVP) results in hyponatremia, a risk factor in pathophysiological states such as cirrhosis. This study tested the hypothesis that changes in the expression of TRPV4, a transient receptor potential channel that has been shown to be activated by osmotic stimulation, in vasopressin neurons contributes to inappropriate vasopressin release in BDL rats. Four weeks after surgery, BDL rats demonstrated significantly increased plasma vasopressin and plasma renin activity (PRA), hypervolemia, and decreased plasma osmolality compared to sham ligated controls. Western Blot analysis revealed that TRPV4 expression was significantly increased in brain punches from BDL rats containing the supraoptic nucleus (SON) (100% ± 11 to 157% ± 4.8), but not the paraventricular nucleus (PVN) of the hypothalamus. Immunohistochemistry analysis demonstrated that TRPV4 is co‐localized in AVP neurons in both PVN and SON. The percentage of AVP neurons expressing TRPV4 was significantly increased (36 % ± 3 to 55.3% ± 4.3) only in the SON of BDL rats. It could be that increased expression of TRPV4 in AVP neurons in the SON resets their osmosensitivity allowing them to continue to release AVP in the face of hypoosmolality and hyponatremia contributing to the pathogenesis of inappropriate AVP release. NIH R01 HL55692