Key result
Long-term smoking was associated with an impaired increase in forearm vascular resistance after L-NMMA compared to nonsmokers (35.6% vs 118.8%, P<0.001), reflecting diminished nitric oxide tone.
Why the study?
Does smoking alter endothelium-dependent control of vascular tone and response to endothelin-1 in clinically healthy men?
Observational (n=45)
Does smoking alter endothelium-dependent control of vascular tone and response to endothelin-1 in clinically healthy men?
Absolute Event Rate: 35.6% vs 118.8%
p-value: p=<.001
Long-term smoking impairs nitric oxide-dependent basal vascular tone and endothelium-dependent vasodilation, while short-term smoking enhances endothelin-1-induced vasoconstriction, suggesting mechanisms for smoking-related atherogenesis.
May link smoking to endothelial dysfunction in vascular disease; leaves open causal mechanisms and therapeutic targets.
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.
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Kiowski et al. (1994) conducted an observational in Clinically healthy smokers (n=45). Smoking (long-term and short-term) vs. Nonsmokers was evaluated on Increase of forearm vascular resistance (FVR) after L-NMMA (p=<.001). Long-term smoking was associated with an impaired increase in forearm vascular resistance after L-NMMA compared to nonsmokers (35.6% vs 118.8%, P<0.001), reflecting diminished nitric oxide tone.
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