Abstract
Angiotensin I converting enzyme activity is detectable in serum and isolated liver granulomas of mice infected with Schistosoma mansoni. At the chronic phase of the infection (20 wk) the intensity of the granulomatous response spontaneously diminishes. Concomitantly, an increase in angiotensin I converting enzyme activity is observed. The objective of this investigation was to determine the source of this elevated angiotensin I converting enzyme activity. In chronically infected mice, measurements showed that angiotensin I converting enzyme activity in hepatic venous blood was higher than that of peripheral venous blood. In contrast, normal mice demonstrated no difference in regional venous angiotensin I converting enzyme activity. Isolated liver granulomas cultured in vitro released angiotensin I converting enzyme into the culture medium. When granulomas were dispersed into single cell suspension, angiotensin I converting enzyme activity was traced to the adherent cell fraction. Both granulomas and adherent cells from granulomas of the chronically (20 wk) infected mice secreted far more angiotensin I converting enzyme than those from animals with acute (8 wk) infection. Cycloheximide partially inhibited enzyme release. We conclude that in murine schistosomiasis, angiotensin I converting enzyme is produced by the granuloma macrophage. The enzyme is released from the granuloma into the circulation probably resulting in increased serum angiotensin I converting enzyme activity. The role of elevated angiotensin I converting enzyme activity within the lesion as well as the circulation remains to be elucidated.
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