This Article Full Text Full Text (PDF) All Versions of this Article: 44/4/392    most recent 01.HYP.0000141484.53649.6fv1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dixon, I. M.C. Articles by Drobic, V. Search for Related Content PubMed PubMed Citation Articles by Dixon, I. M.C. Articles by Drobic, V. Related Collections Remodeling Hypertrophy

(Hypertension. 2004;44:392.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

Gender Dependency in the Pathogenesis of Cardiac Hypertrophy

Effect of Norepinephrine on Transforming Growth Factor-ß Release in Female Heart

From the Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre and Department of Physiology, University of Manitoba, Winnipeg, Canada.

Correspondence to Ian M.C. Dixon, PhD, Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, 351 Tache Ave, Winnipeg, Manitoba, Canada R2H 2A6. E-mail idixon@sbrc.ca

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Representing the most numerous nonmyocytes in the myocardium, adult cardiac fibroblasts (and myofibroblasts) function to synthesize fibrillar collagens and thus maintain the integrity of the cardiac extracellular matrix (matrix). Matrix remodeling is manifest as interstitial fibrosis of the remnant heart or the progressive evolution of the structure of the infarct scar in the etiology of post-myocardial infarction heart failure.¹ In normal heart tissue, matrix protein secretion and deposition is carried out exclusively by cardiac fibroblasts with relatively low turnover of proteins, whereas contractile and hypersynthetic myofibroblasts are the relevant phenotypic variant in wound healing² or in hypertrophied and failing hearts.^3,4 Much of the current literature that addresses cardiac fibroblast or myofibroblast function deals with the effects of a limited number of profibrotic factors and infrequently addresses the interplay of these stimuli. Whereas interstitial fibrosis is a component of cardiac hypertrophy and contributes to the development of heart failure and norepinephrine stimulation of nonmyocytes is linked to the activation of collagen genes, the precise mechanisms of cardiac myofibroblast activation by this ligand are not well understood.

Recently, a direct relation between increased sympathetic activity and hypertensive left ventricular hypertrophy was demonstrated in a small human cohort (notably, 35% of these patients were female).⁵ Indeed, ß-blockers are again among the agents of choice in the clinician’s armament for treatment of cardiac hypertrophy and heart failure.⁶ In contrast, -blockers have attracted relatively little attention in the clinical setting. Despite the association between plasma norepinephrine and incidence of maladaptive cardiac hypertrophy, the role of . . . [Full Text of this Article]

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