Table of Contents
Advances in Endocrinology
Volume 2014 (2014), Article ID 179795, 6 pages
Research Article

Angiotensin II, Vasopressin, and Collagen-IV Expression in the Subfornical Organ in a Case of Syndrome of Inappropriate ADH

1Departamento de Anatomía, Anatomía Patológica e Histología, Facultad de Medicina, Universidad de La Laguna, Ofra s/n, 38071 La Laguna, Tenerife, Spain
2Departamento de Biotecnología, Instituto de Investigación y Ciencias de Puerto del Rosario, C/Tenerife 35, 35600 Puerto del Rosario, Fuerteventura, Isla Canarias, Spain
3Departamento de Farmacología, Facultad de Medicina, Universidad de La Laguna, Ofra s/n, 38071 La Laguna, Tenerife, Islas Canarias, Spain

Received 28 May 2014; Revised 28 July 2014; Accepted 19 August 2014; Published 6 November 2014

Academic Editor: Carole Samango-Sprouse

Copyright © 2014 Emilia M. Carmona-Calero et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The syndrome of inappropriate antidiuretic hormone (SIADH) is a disease characterized by hyponatremia and hyperosmolarity of urine where vasopressin and angiotensin II are implicated in the alteration of salt water balance and cardiovascular and blood pressure regulation. The aim of this study is to analyse the expression of substances related with cardiovascular and salt water regulation in the subfornical organ in a case of SIADH. Two brains, one taken from a 66-year-old man with SIADH and the other from a 63-year-old man without SIADH, were used. Immunohistochemical study was performed using anti-angiotensin II, anti-vasopressin, and anti-collagen-VI as primary antibodies. Angiotensin and vasopressin immunoreaction were found in neurons, in perivascular spaces, and in the ependymal layer in the subfornical organ in both cases. However, in the SIADH case, the angiotensin II and collagen-IV expression in the SFO were different suggesting this organ’s possible participation in the physiopathology of SIADH.