Captopril does not blunt the sympathoadrenal response to cigarette smoking in normotensive humans.

The aim of this study was to assess whether an interaction exists between the renin-angiotensin system and the sympathetic nervous system at the level of the adrenal medulla during smoking in normal humans. Thirteen habitual smoking volunteers were studied in a randomized, single-dose, double-blind, cross-over fashion using 50 mg captopril vs placebo followed by smoking of two high nicotine content cigarettes within 15 min. Blood samples were obtained at frequent intervals before, during and after smoking. We found that the increase in plasma adrenaline concentration during cigarette smoking was modest. There was no difference between captopril treatment as compared to placebo. Thus, the adrenaline response to cigarette smoking was not blunted by acute blockade of angiotensin II generation. A significant increase in heart rate, and blood pressure was found as well. No increase in plasma noradrenaline concentration was found. Plasma renin concentration increased significantly during captopril treatment, whereas it decreased throughout the study period in the placebo phase. Plasma angiotensin II concentration decreased in both the captopril treatment and the placebo phase throughout the study period, but this was more pronounced during captopril treatment. In conclusion, cigarette smoking-induced activation of the sympathetic nervous system was not blunted by acute ACE-inhibition by captopril. This indicates that angiotensin II does not facilitate smoking-induced activation of sympathoadrenal activity in humans.