Abstract
Angiotensin I-converting enzyme (ACE, EC 3.4.15.1.) was measured in serum and in pulmonary plasma membranes of 140 spontaneously hypertensive rats (SHR, Okamoto Aoki strain), divided into 4 groups, and treated with SQ 14225 (Captopril®), 0.2 mg · ml −1 in drinking water, for 0–24 weeks. Serum ACE activity increased 2.5–3 fold after 12–24 weeks of SQ 14225 treatment, paralleled by an increasep of ACE concetration in purified pulmonary plasma membranes (25–52%), and in ACE concentration upon solubilization with Triton X-100 from such plasma membranes (96–120%). We conclude that the ACE inhibitor, SQ 14225, causesp marked induction of pulmonary ACE biosynthesis. High serum ACE activity probably reflects increased total biosynthesis of the enzyme.
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