Circulation, Vol 90, 27-34, Copyright © 1994 by American Heart Association
W Kiowski, L Linder, K Stoschitzky, M Pfisterer, D Burckhardt, F Burkart and FR Buhler
BACKGROUND: Smoking is a major risk factor for the development of
atherosclerosis. Because endothelial dysfunction may be a marker for future
atherosclerosis, we investigated the effects of smoking on
endothelium-dependent control of vascular tone. METHODS AND RESULTS: The
effects of brachial arterial infusions of NG-monomethyl-L-arginine
(L-NMMA), a nitric oxide synthesis inhibitor; sodium nitroprusside;
endothelin-1; and norepinephrine on forearm blood flow (strain-gauge
plethysmography) were compared in 29 long-term smokers and 16 nonsmokers.
The acute effects of smoking on systemic hemodynamics, plasma
catecholamines, and forearm vascular responses to these compounds were
investigated in smokers only. Smokers did not differ from nonsmokers (n =
16) regarding the vascular effects of sodium nitroprusside (n = 13) or
vasoconstriction due to norepinephrine and endothelin-1 (n = 16). Low-dose
endothelin-1-induced vasodilation, believed to reflect endothelial
prostacyclin or nitric oxide release, was absent in smokers (n = 16), and
their increase of forearm vascular resistance (FVR) after L-NMMA (n = 13)
was impaired (35.6 +/- 27.9% versus 118.8 +/- 43.2%, P < .001).
Short-term smoking (n = 11) increased blood pressure, heart rate, and
plasma epinephrine concentrations (P < .05 or less); enhanced
endothelin-1-induced vasoconstriction (delta FVR, 457 +/- 192% versus 254
+/- 143%, P < .01); and decreased norepinephrine-induced
vasoconstriction (P < .05), but had no effect on the other
interventions. CONCLUSIONS: Long-term smoking is associated with a
diminished nitric oxide-dependent component of basal vascular tone and an
impaired endothelium-dependent vasodilator response to low-dose
endothelin-1 and short-term smoking enhances endothelin-1-induced
vasoconstriction. Impaired endothelial control of vascular tone might
reflect impairment of normal antiatherosclerotic endothelial functions in
smokers, but the relevance of smoking-induced enhancement of endothelin-1
vasoconstriction remains to be determined.
ARTICLES
Diminished vascular response to inhibition of endothelium-derived nitric oxide and enhanced vasoconstriction to exogenously administered endothelin-1 in clinically healthy smokers
Division of Cardiology, University Hospital of Zurich, Switzerland.
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