In this regard, it has recently been shown that mice with renal angiotensin I-converting enzyme (ACE) deficiency but normal plasma ACE activity were protected against angiotensin II-induced [26] as well as N(ω)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension [25]. This evidence concerns the gene ACE and hyperinsulinemic hypoglycemia, familial, 4.