Abstract-ACE plays an important role in the regulation of arterial pressure; however, a linear relationship between ACE expression and arterial pressure has not been demonstrated. The present study employed telemetric monitoring in female transgenic mice to determine the influence of partial and complete deletion of the ACE gene on basal arterial pressure and arterial pressure responses to a high-NaCl diet. On the basal NaCl diet, 24-hour mean arterial pressure was significantly correlated with the number of functional copies of the ACE gene; ie, arterial pressure was lowest in 0-copy (80Ϯ1 mm Hg), intermediate in 1-copy (100Ϯ1 mm Hg), and highest in 2-copy (113Ϯ1 mm Hg) ACE mice. The high-NaCl diet significantly increased mean arterial pressure in 0-copy (99Ϯ1 mm Hg) and 1-copy (108Ϯ1 mm Hg) mice but not in 2-copy mice (114Ϯ1 mm Hg). These results demonstrate a copy-dependent relationship between ACE gene expression and both basal arterial pressure and arterial pressure responses to a high-NaCl diet, suggesting that either partial or complete reduction in the ACE gene can alter arterial pressure. Key Words: angiotensin-converting enzyme Ⅲ arterial pressure Ⅲ renin-angiotensin system Ⅲ sodium T he ACE is a dipeptidyl carboxy-peptidase that both converts the inactive decapeptide angiotensin I to the active octapeptide angiotensin II and inactivates bradykinin by degradative metabolism. These metabolic events promote increased arterial pressure, sympathetic nervous system activity, sodium retention, and mitogenesis of vascular cells. Because of these prohypertensive effects, many pharmacological treatments for hypertension have focused on the inhibition of ACE activity.Homologous recombination techniques have been used to test the cardiovascular effects of altering expression of components of the renin-angiotensin system. Deletion of either the angiotensinogen 1,2 or angiotensin type 1 (AT 1a ) receptor 3 gene decreases arterial pressure in a copy-dependent manner, indicating a direct relationship between arterial pressure and the number of functional gene copies. In contrast, studies in ACE knockout mice have reported that although deletion of both copies of the ACE gene significantly reduces basal arterial pressure, 4,5 deletion of a single copy of the ACE gene has no effect on basal arterial pressure. 4,5 These reports suggest that arterial pressure is not influenced by partial decreases in ACE gene expression, a finding consistent with the common assumption that ACE is not rate-limiting in the renin-angiotensin system.The interpretation of these results is limited by the relatively low sensitivity of the methods that were used to record arterial pressure, ie, tail-cuff 4,6 and acute catheterization. 5