Circulation, Vol 90, 248-253, Copyright © 1994 by American Heart Association
G Grassi, G Seravalle, DA Calhoun, GB Bolla, C Giannattasio, M Marabini, A Del Bo and G Mancia
BACKGROUND: The pressor and tachycardic effects of cigarette smoking are
associated with an increase in plasma catecholamines, suggesting the
dependence of these effects on adrenergic stimulation. Whether the
stimulation occurs at a central or a peripheral level and whether reflex
mechanisms are involved is unknown. METHODS AND RESULTS: In nine
normotensive healthy subjects (age, 33.0 +/- 3.5 years, mean +/- SEM), we
measured blood pressure (Finapres device), heart rate (ECG), calf blood
flow and vascular resistance (venous occlusion plethysmography), plasma
norepinephrine and epinephrine (high-performance liquid chromatography
assay), and postganglionic muscle sympathetic nerve activity
(microneurography from the peroneal nerve) while subjects were smoking a
filter cigarette (nicotine content, 1.1 mg) or were in control condition.
Cigarette smoking (which raised plasma nicotine measured by
high-performance liquid chromatography from 1.0 +/- 0.9 to 44.2 +/- 7.1
ng/mL) markedly and significantly increased mean arterial pressure (+13.2
+/- 2.3%), heart rate (+30.3 +/- 4.7%), calf vascular resistance (+12.1 +/-
4.9%), plasma norepinephrine (+34.8 +/- 7.0%), and plasma epinephrine
(+90.5 +/- 39.0%). In contrast, muscle sympathetic nerve activity showed a
marked reduction (integrated activity -31.8 +/- 5.1%, P < .01). The
reduction was inversely related to the increase in mean arterial pressure
(r = -.67, P < .05), but the slope of the relation was markedly less
(-54.1 +/- 7.5%, P < .05) than that obtained by intravenous infusion of
phenylephrine in absence of smoking. The hemodynamic and neurohumoral
changes were still visible 30 minutes after smoking and occurred again on
smoking a second cigarette. Sham smoking was devoid of any hemodynamic and
neurohumoral effect. CONCLUSIONS: These data support the hypothesis that in
humans the sympathetic activation induced by smoking depends on an
increased release and/or a reduced clearance of catecholamines at the
neuroeffector junctions. Central sympathetic activity is inhibited by
smoking, presumably via a baroreceptor stimulation triggered by the
smoking-related pressor response. The baroreflex is impaired by smoking,
however, indicating that partial inability to reflexly counteract the
effect of sympathetic activation is also responsible for the pressor
response.
ARTICLES
Mechanisms responsible for sympathetic activation by cigarette smoking in humans
Cattedra Medicina Interna, Ospedale S. Gerardo dei Tintori, Monza, Italy.
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