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Receptor binding occurrence and plasma levels of natriuretic peptides in response to sympathectomy
Author(s) -
Hansson Magnus
Publication year - 2005
Publication title -
microscopy research and technique
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 118
eISSN - 1097-0029
pISSN - 1059-910X
DOI - 10.1002/jemt.20192
Subject(s) - medicine , endocrinology , npr2 , sympathectomy , receptor , npr1 , endocardium , atrial natriuretic peptide , natriuretic peptide , blood pressure , sympathetic nervous system , chemistry , heart failure
In the present investigation the relationship between the sympathetic nervous system and the endocardial levels of receptor binding sites for natriuretic peptides and the plasma content of atrial natriuretic peptide were analyzed in rats. In order to destruct the cardiac sympathetic nerve terminals, chemical sympathectomy with 6‐hydroxydopamine was made in parallel with intravenous measurements of blood pressure and heart frequency. By use of immunohistochemical and enzyme‐linked‐immunosorbent techniques the expression of tyrosine hydroxylase‐positive sympathetic nerve terminals and plasma levels of pro‐atrial natriuretic peptide were determined, respectively. The occurrence of receptor binding sites for natriuretic peptides was examined by in vitro receptor autoradiography. In contrast to the marked occurrence of natriuretic peptide receptor binding sites seen in the ventricular endocardium of control rats, the sympathectomized rats exhibited a decreased number of binding sites for natriuretic peptides in the endocardium of both the right and left chambers. Interestingly, this was found in parallel with a significant decrease of systolic and diastolic blood pressure and increased plasma levels of pro‐atrial natriuretic peptide in the treated group of rats. These findings, together with those in previous studies, give support to an idea that one part of the blood pressure‐decreasing effects, seen in patients treated with β‐adrenergic blockade, might be through a reduction of the natriuretic clearance receptor C, then giving rise to increased levels of atrial natriuretic peptide. Microsc. Res. Tech. 67:90–99, 2005. © 2005 Wiley‐Liss, Inc.