PRESSURE-INDUCED AND VOLUME-INDUCED LEFT-VENTRICULAR HYPERTROPHIES ARE ASSOCIATED WITH DISTINCT MYOCYTE PHENOTYPES AND DIFFERENTIAL INDUCTION OF PEPTIDE GROWTH-FACTOR MESSENGER-RNAS

Background Chronic pressure and volume ocerload (PO and VO) result in morphologically and functionally distinct forms of myocardial hypertro phy. 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 m RNA levels were quantified in LV myocardium from rats with LV hypertro phy due to PO or VO caused by suprarenal aortic constriction or an abd ominal aortocaval fistula, respectively, for 1 week. Although PO and V O caused comparable increases in LV weight and preproatrial natriureti c factor mRNA, PO but not VO increased mRNA levels for the fetal genes beta-myosin heavy chain and skeletal alpha-actin and reduced the mRNA level of sarcoplasmic reticulum Ca2+ ATPase. In a myocyte-enriched my ocardial fraction, transforming growth factor-beta(3) 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 wit h VO. In a nonmyocyte-enriched myocardial fraction, transforming growt h factor-p, and insulin-like growth factor-1 mRNA levers were decrease d with VO but unchanged with PO. Conclusions PO- and VO-induced LV hyp ertrophies are associated with distinct molecular phenotypes and patte rns of peptide growth factor induction. Stimulus-specific heterogeneit y in the signaling events and peptide growth factors coupled to gene e xpression could play a role in determining the type of hypertrophy tha t is caused by various forms of hemodynamic overload.