Why the study?
Does smoking increase angiotensin-converting enzyme activity in intact human alveolar macrophages?
Does smoking increase angiotensin-converting enzyme activity in intact human alveolar macrophages?
Smoking is associated with increased angiotensin-converting enzyme activity in intact human alveolar macrophages.
May support smoking-related pulmonary angiotensin II increase; hypothesis-generating in this level 5 model and leaves clinical relevance open.
Serum angiotensin-converting enzyme (ACE) activity is known to be elevated in various granulomatous conditions such as sarcoidosis, whose characteristic epithelioid cells are thought to belong to the macrophage series. It was recently shown that alveolar macrophages had ACE activity in their sonicated and homogenate forms. We investigated ACE activity of human alveolar macrophages in the intact form using a sensitive radioimmunoassay of generated angiotensin II. We also investigated the effect of smoking on ACE activity of alveolar macrophages using this method. Alveolar macrophages generated angiotensin II (218 +/- 106 pg/20 min/10(5) cells). More angiotensin II was generated in smokers (246 +/- 119 pg/20 min/10(5) cells) than in nonsmokers (160 +/- 50 pg/20 min/10(5) cells) (p less than 0.05). These data showed that ACE activity of macrophages is higher in smokers than nonsmokers.
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Sugiyama et al. (2009) studied this question.
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