(Circulation. 1995;92:2385-2390.)
© 1995 American Heart Association, Inc.
Articles |
Pressure- and Volume-Induced Left Ventricular Hypertrophies Are Associated With Distinct Myocyte Phenotypes and Differential Induction of Peptide Growth Factor mRNAs
From the Cardiomyopathy Center and Cardiovascular Division, Departments of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass.
Correspondence to Dr Wilson S. Colucci, Cardiomyopathy Center and Cardiovascular Division, Boston University Medical Center, 88 E Newton St, Boston, MA 02118.
Background Chronic pressure and volume overload (PO and VO) result in morphologically and functionally distinct forms of myocardial hypertrophy. We tested the hypothesis that PO- and VO-induced left ventricular (LV) hypertrophies are associated with distinct molecular phenotypes and patterns of peptide growth factor induction.
Methods and Results mRNA levels were quantified in LV
myocardium from rats with LV hypertrophy due to
PO or VO caused by suprarenal aortic constriction or an abdominal
aortocaval fistula, respectively, for 1 week. Although PO and VO caused
comparable increases in LV weight and prepro–atrial
natriuretic factor mRNA, PO but not VO increased mRNA
levels for the fetal genes ß-myosin heavy chain and skeletal
-actin and reduced the mRNA level of sarcoplasmic reticulum
Ca2+ATPase. In a myocyte-enriched myocardial
fraction, transforming growth factor-ß3 and
insulin-like growth factor-1 mRNA levels were increased with PO but
not VO; acidic fibroblast growth factor mRNA was unchanged with PO but
decreased with VO. In a nonmyocyte-enriched myocardial
fraction, transforming growth factor-ß3 and
insulin-like growth factor-1 mRNA levels were decreased with VO but
unchanged with PO.
Conclusions PO- and VO-induced LV hypertrophies are associated with distinct molecular phenotypes and patterns of peptide growth factor induction. Stimulus-specific heterogeneity in the signaling events and peptide growth factors coupled to gene expression could play a role in determining the type of hypertrophy that is caused by various forms of hemodynamic overload.
Key Words: hypertrophy • myocardium • genes • RNA • growth substances
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