Left Ventricular Regional Variations in Myosin Isoform Shift in Dahl Salt-Sensitive Hypertensive Rats.

Abstract

To evaluate the effects of chronic pressure overload on different parts of the left ventricle (LV), we examined a myosin isoform shift from V1 to V3 as a biochemical marker of LV hypertrophy in Dahl salt-sensitive (DS) rats. Six-week-old DS rats were fed an 8% (high salt, HS; n 24) or a 0.3% (low salt, LS; n 12) NaCl diet. After 2 or 4 weeks, the hearts were dissected and the LVs were separated into four parts (the base and mid- after blood pressure is controlled (12). Studies have confirmed this prominence of the basal septal hypertrophy in hypertensives, and especially in elderly hypertensives (13,14). These observations suggest that myocardial hypertrophy as a response to pressure overload may develop differently at individual regions of the left ventricle (LV). Thus, we surmised that the base of the IVS is exposed to the greatest pressure overload, and that LVH begins at this site in hypertensive patients. Using the transformation of the myosin isoform from V1 to V3 as a biochemical marker of pressure overload, the present study was carried out to determine which part of the ventricular wall is most stressed by systemic hypertension in Dahl salt-sensitive rats (DS). MethodsSix-week-old male inbred DS rats (n 36) were obtained

Attenuation of MicroRNA‐22 derepressed PTEN to effectively protect rat cardiomyocytes from hypertrophy

“…These results suggested that miR‐22 might be partial responsible for PE‐ or Ang II‐induced hypertrophy. As previous reports, besides specific hypertrophic markers, nppa and myh6 also had important roles in mediating cardiac hypertrophy (Sakurai et al, 2003). Considering the effects of miR‐22 on regulating nppa and myh6 expression, we speculated that the effects of miR‐22 in regulating cardiomyocyte hypertrophy might be partially through regulating the expression of nppa and myh6 .…”