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Effect of AT sub(2) blockade on cardiac hypertrophy as induced by high dietary salt in the proatrial natriuretic peptide (ANP) gene-disrupted mouse
The role of the angiotensin II type 2 receptor (AT sub(2)) during alterations in cardiac size remains largely unclear. Through employment of an AT sub(2) antagonist, the present study explored a possible involvement of the AT sub(2) receptor during salt-induced cardiac hypertrophy in the proatrial n...
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Published in: | Canadian journal of physiology and pharmacology 2006-06, Vol.84 (6), p.625-634 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Online Access: | Get full text |
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Summary: | The role of the angiotensin II type 2 receptor (AT sub(2)) during alterations in cardiac size remains largely unclear. Through employment of an AT sub(2) antagonist, the present study explored a possible involvement of the AT sub(2) receptor during salt-induced cardiac hypertrophy in the proatrial natriuretic peptide gene-disrupted mouse (ANP super(-/-)). ANP super(-/-) mice received either saline solution or the AT sub(2) antagonist, PD123319, and were then placed on a high salt diet (8.0% NaCl) for 3A weeks. Cardiac and pulmonary size, expression of the renin-angiotensin system (RAS), and the behaviour of various hypertrophy marker genes were assessed. PD123319 caused enhanced expression of the systemic RAS, yet the cardiac RAS was largely unaffected. Although AT sub(2) blockade did not alter whole cardiac mass, right ventricle mass, as well as pulmonary mass-to-body mass ratios were significantly decreased. Collagen type I was decreased in the latter tissues, likely contributing to the regression in mass.Original Abstract: le role du recepteur AT sub(2) durant les modifications de la taille du coeur est encore mal connu. la presente etude a examine, au moyen d'un antagoniste AT sub(2), une influence possible du recepteur AT sub(2) durant l'hypertrophie cardiaque induite par le sel chez la souris au gene proANP inactive (ANP super(-/-)). Les souris ANP super(-/-) ont recu une solution physiologique salee ou l'antagoniste AT sub(2), PD123319, puis ont ete soumises a un regime sode (8,0 % NaCl) pendant 3 semaines. la taille du coeur et des poumons, l'expression du systeme renine-angiotensine (SRA) et le comportement de divers genes marqueurs d'hypertrophie cardiaque ont ete evalues. PD123319 a cause une augmentation de l'expression du SRA systemique, mais a eu tres peu d'effet sur le SRA cardiaque. le blocage de AT sub(2) n'a pas modifie le poids total du coeur et du ventricule gauche, mais les rapports poids pulmonaire-poids corporel ont considerablement diminue. le collagene de type 1 de ces tissus a diminue, ce qui a probablement contr Mots-cles : souris inactives pour le peptide natriuretique auriculaire, hypertrophie cardiaque, systeme renine-angiotensine, recepteur AT sub(2), sensibilite au sel.[Traduit par la Redaction] |
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ISSN: | 0008-4212 1205-7541 |
DOI: | 10.1139/Y06-016 |