Angiotensin II inhibition of mitogen- and antigen-induced human blood mononuclear cell thymidine uptake.

Angiotensin-converting enzyme and other components of the angiotensin system may participate in the regulation of inflammation. We therefore studied the effects of angiotensin II on human mononuclear cell reactivity. 48 hr phytohemagglutinin (5 micrograms/ml)-stimulated cultures of mononuclear cells from 6 subjects revealed thymidine uptake of 84,525 +/- 18,923 cpm (mean +/- se). When cultures contained angiotensin II (10(-7) M), reactivity was decreased to 75,279 +/- 17,727 cpm (p less than 0.05, paired t-test). Depletion of monocytes by nylon wool filtration or Percoll density-gradient centrifugation revealed persistence of the effect. Tetanus toxoid (0.5 LfU/ml)-induced thymidine uptake (86,910 +/- 31,591 cpm) was also reduced by the presence of 10(-6) M angiotensin II (68,094 +/- 25,509 cpm, p less than 0.01, paired t-test) when angiotensin II was added on the fourth day of 5 day cultures. No angiotensin II effects were observed on unstimulated thymidine incorporation. These findings indicate that angiotensin II can inhibit antigen- and mitogen-induced mononuclear cell reactivity and suggest that angiotensin II, the product of angiotensin converting enzyme may be an inhibitor of human lymphocyte function.