Vasopressor systems during smoking in humans.

In this study we correlated the effects of cigarette smoking on the activity of vasopressor systems in humans with changes in heart rate and blood pressure and compared them with changes observed after physical exercise or graded norepinephrine infusion. No relationship was established between changes in either plasma angiotensin II or vasopressin concentration and the hemodynamic parameters, although there was a small increase in both hormones during smoking. In contrast, heart rate (r = -0.245, p less than 0.01, n = 136) was negatively related to plasma norepinephrine concentration during the smoking of five cigarettes. A comparable, negative correlation, although much closer, was found during graded norepinephrine infusion between heart rate and norepinephrine concentration (r = -0.682, p less than 0.001), whereas both parameters were positively related under conditions of physical exercise (r = 0.866, p less than 0.001). In an attempt to block the assumed nicotine-induced sympathetic stimulation, smoking experiments were carried out after acute beta blockade (200 mg metoprolol orally). There was a parallel shift of heart rate and blood pressure to lower values. However, beta blockade did not abolish the smoking-induced rise in blood pressure and heart rate. At the present time no direct evidence is available for a nicotine-induced increase of norepinephrine concentration at postsynaptic receptors during smoking in humans.(ABSTRACT TRUNCATED AT 250 WORDS)