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Effects of arginine vasopressin deficiency on innate immunity in the rat
Author(s) -
QuintanarStephano Andrés,
ViñuelaBerni Verónica,
OrganistaEsparza Alejandro,
TinajeroRuelas Manuel,
HuertaCarreón Erika,
Kovacs Kalman,
Berczi Istvan
Publication year - 2015
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.29.1_supplement.634.3
Subject(s) - evans blue , vasopressin , medicine , endocrinology , histamine , extravasation , vasopressin receptor , vasopressin antagonists , innate immune system , vascular permeability , receptor , antagonist , immunology
Immune and vascular endothelial cells possess arginine vasopressin (AVP) receptors. AVP is an important stimulating/regulatory hormone in acquired immunity, whereas its role on innate immunity (INIM) is not well known. Neurointermediate pituitary lobectomy (NIL) in the rat causes permanent low AVP serum levels. Here, we investigate the AVP and INIM relationship in NIL rats (3 weeks after surgeries) subject to INIM tests: Phagocytic index (PI) (peritoneal macrophages (M θ ) erytrophagocytosis), and Skin Evans blue extravasation‐histamine doses‐response test. In the Study 1, NIL group was compared against Intact control (IC), sham operated (SHAM) and anterior pituitary lobectomysed (AL) groups. In the study 2, NIL group was compared against IC, NIL+desmopressin (a synthetic analog of AVP) and IC+conivaptan (antagonist of V1a‐V2 AVP receptors) groups. Results: Study 1 showed that as compared with the IC and AL groups, PI was significant decreased in NIL animals. In the Evans blue extravasation‐histamine test study, a significant and similar increases of skin edema histamine doses‐dependent occurred in NIL and IC+conivaptan groups, whereas no significant differences in IC and NIL+desmopressin groups were appreciated. Conclusion AVP plays an important role in phagocytic activity of the peritoneal M θ and for the stabilization of the vascular endothelial cells permeability during histamine inflammation. Supported by UAA‐PIFF 14‐1. Universidad Autónoma de Aguascalientes, México and the Jarislowsky and Lloyd Carr‐Harris Foundations.