This study utilized a model of pressure overload cardiac hypertrophy in the mouse to test the hypothesis that ACE gene expression was regulated differentially in heart, kidney and lung during the development and maintenance of cardiac hypertrophy. The suprarenal descending aorta of CD-1 mice of both sexes with body weights (BW) between 25 and 30 g was ligated around a 28 gauge needle in order to establish a 40-50% coarctation (DAC). One, 7 and 28 days later, mean arterial pressure (MAP) was measured in conscious unrestrained mice via a carotid cannula. Mice were sacrificed by neck dislocation and heart weight to BW ratio (Ht/BW, mg/g) was obtained. Total RNA was extracted from heart, kidney and lung for measurement of ACE mRNA levels by slot blot analysis and standardized with ISSrRNA Results (mean+SEM, n=5-11) are: MAP Ht/BW ACE mRNA /18S rRNA ratios (mmHg) (mg/g) Heart Kidney Lung Sham 112±2 4.6+0.0 100±11 100±13 100± 7 1-day 125±2 4.5+0.0 88±10 81±8 120±14 7-day 131 ±5 5.±0.0 193+20 200+14 112+15 28-day 131 ±5 5.2+0.0 188±25 128±14 91+8 p<0.05, compared to respective values of sham controls. Our data indicate that ACE gene expression in heart, but not in kidney and lung, is highly correlated with the development and maintenance of the pressure overload induced cardiac hypertrophy (r=0.05. p<0.01). This pressure overload hypertrophy model in mice may serve as a very useful model to study the role of renin-angiotensin system in the development of hypertrophy and/or heart failure.