Why the study?
Does captopril treatment alter the tissue distribution and activity of angiotensin converting enzyme in rats?
Does captopril treatment alter the tissue distribution and activity of angiotensin converting enzyme in rats?
Captopril treatment in rats significantly increases ACE activity in serum and pulmonary tissue, suggesting the lungs are the primary source of increased serum ACE during ACE inhibitor therapy.
Observed compensatory ACE upregulation with captopril in rats; leaves open relevance to human dosing or efficacy.
Effect on different tissues with regard to angiotensin converting enzyme during captopril treatment in the rat was studied. Male Wistar-Kyoto rats (n = 9) were treated during four weeks with captopril dissolved into the drinking water at the dose 30 mg/kg/day. Control rats (n = 9) had water only. Serum angiotensin converting enzyme (ACE) activity increased three-fold during captopril treatment, and ACE of purified pulmonary plasma membranes increased about 64% (P less than 0.001) compared to untreated rats. ACE activity of membrane fractions of other tissues studied i.e. testicles, epididymes, kidneys, and small intestine brush border did not increase similarly during captopril treatment. The highest amounts of ACE was demonstrated in epididymes, but captopril did not produce increased amounts of ACE in the epididymes. The main source of increased serum ACE activity during captopril treatment appeared to be in the pulmonary tissue.
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Forslund et al. (1984) studied this question.
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