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Mikhail Samsonov, MD; Eugeney Nassonov, MD
Moscow, Russia

Gabriele Werner-Felmayer, PhD; Dietmar Fuchs, PhD; Helmut Wachter, PhD
Innsbruck, Austria

Arch Intern Med. 1993;153(9):1138-1142.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Captopril is used as an antihypertensive drug for its inhibiting effect on angiotensin-converting enzyme, the enzyme that converts inactive angiotensin I to the active vasopressor angiotensin II. Captopril has also been shown to induce immunosuppression by a mechanism that involves monocytes and CD8⁺ cells. In vivo, captopril was beneficial in patients with rheumatoid arthritis² and in an animal model of systemic lupus erythematosus.³

To study whether captopril has any direct effects on cells of the monocyte/macrophage lineage, we tested its influence on formation of neopterin, an in vivo marker for immune activation,⁴ and on tryptophan degradation. Both biochemical pathways are induced by interferon gamma in macrophages.⁵ We used the human myelomonocytic cell line THP-1 (American Type Culture Collection, Rockville, Md) that behaves similarly in this respect to freshly isolated monocytes.⁶ Cells grown in RPMI 1640 containing 10% heat-inactivated fetal calf serum, 2 mmol/L of L-glutamine, . . . [Full Text PDF of this Article]

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