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Cardiovascular Research 2007 76(2):311-322; doi:10.1016/j.cardiores.2007.06.033
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Copyright © 2007, European Society of Cardiology

Smoking accelerates the progression of hypertension-induced myocardial hypertrophy to heart failure in spontaneously hypertensive rats*

K. Meurrensa, S. Rufb, G. Rossb, R. Schleefc, K. von Holtd and K.-D. Schlüterb,*

aPhilip Morris Research Laboratories bvba, Leuven, Belgium
bJustus-Liebig-Universität Giessen, Physiologisches Institut, Germany
cPhilip Morris USA, Inc., Richmond, Virginia, USA
dPhilip Morris Research Laboratories GmbH, Cologne, Germany

*Corresponding author. Justus-Liebig-Universität, Physiologisches Institut, Aulweg 129, D-35392 Giessen, Germany. Tel.: +49 641 99 47 212; fax: +49 641 99 47 219. Klaus-Dieter.Schlueter{at}physiologie.med.uni-giessen.de

Objective Myocardial hypertrophy often develops in response to hypertension, and it is causal to and an independent predictor of heart failure. Several risk factors modify the progression of hypertrophy, the associated progressive impairment of myocardial function, and eventually the transition to overt congestive heart failure. The aim of the present study was to investigate the effects of smoking on the progression of pressure-dependent myocardial hypertrophy.

Methods Spontaneously hypertensive rats (SHR) were used as a model for pressure-dependent hypertrophy. SHR were exposed to mainstream smoke from the Kentucky reference cigarette 2R4F (450 µg total particulate matter/l) or to fresh air (control), 5 days a week, twice for 1 h per day with a 30-minute fresh air exposure break for 30, 60, or 90 days. Endpoints for hypertrophy-associated changes were heart weight to body weight ratio, ventricular expression of hypertrophy-associated genes, ischemic tolerance, and inotropic responsiveness to isoprenaline in post-ischemic hearts.

Results Smoke-exposed SHR showed a significant elevation in heart weight to body weight ratio, increased mRNA expression of atrial natriuretic factor (ANF), transforming growth factor (TGF)-β1, ornithine decarboxylase (ODC), and parathyroid hormone-related protein in both ventricles compared to controls. Hearts from smoke-exposed SHR showed a reduced recovery after 30 min global ischemia during the first 5 min of reperfusion and loss of inotropic stimulation after 30 min reperfusion. Smoke cessation was sufficient to reverse most of these alterations. WKY exposed to smoke did not develop similar changes.

Conclusion Our data indicate that several aspects of myocardial hypertrophy are accelerated by smoking.

KEYWORDS Ischemia; Reperfusion; ODC; PTHrP; TGF-β1

* Guy Vassort, INSERM, Montpelier, France, served as Guest Editor for this article.


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