Effect of nicotine on endothelium-dependent arteriolar dilatation in vivo

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Abstract

Smoking is a primary risk factor in coronary and peripheral vascular disease. However, the precise component of cigarette smoke that contributes to the pathogenesis of vascular disease remains unclear. The goal of this study was to determine the effect of nicotine on endothelium-dependent dilatation of peripheral resistance arterioles in vivo. We measured the diameter of resistance arterioles (~50 μm in diameter) contained within the microcirculation of the hamster cheek pouch in response to endothelium- dependent (acetylcholine and ADP) and -independent (nitroglycerin) agonists before and after an intravenous infusion of vehicle or two concentrations of nicotine. Acetylcholine, ADP, and nitroglycerin produced a dose-related dilatation of the cheek pouch arterioles under control conditions. Endothelium-dependent, but not -independent, dilatation of arterioles was modestly impaired by an infusion of a low concentration of nicotine (1.0 μg·kg-1·min-1). Infusion of a higher concentration of nicotine (2 μg·kg-1·min-1), which increased the plasma level of nicotine to 14 ± 1.6 ng/ml, produced a profound selective impairment in endothelium-dependent vasodilatation. We suggest that elevations in plasma nicotine may contribute to the pathogenesis of the peripheral vascular disease observed in smokers.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume272
Issue number5 41-5
StatePublished - Jun 17 1997

Fingerprint

Nicotine
Endothelium
Dilatation
Arterioles
Peripheral Vascular Diseases
Cheek
Nitroglycerin
Adenosine Diphosphate
Acetylcholine
Microcirculation
Vascular Diseases
Intravenous Infusions
Vasodilation
Smoke
Tobacco Products
Cricetinae
Vascular Resistance
Smoking

Keywords

  • acetylcholine
  • adenosine 5'-diphosphate
  • arterioles
  • cheek pouch
  • endothelium-derived relaxing factor
  • hamsters
  • nitric oxide
  • nitroglycerin
  • smoking

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

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abstract = "Smoking is a primary risk factor in coronary and peripheral vascular disease. However, the precise component of cigarette smoke that contributes to the pathogenesis of vascular disease remains unclear. The goal of this study was to determine the effect of nicotine on endothelium-dependent dilatation of peripheral resistance arterioles in vivo. We measured the diameter of resistance arterioles (~50 μm in diameter) contained within the microcirculation of the hamster cheek pouch in response to endothelium- dependent (acetylcholine and ADP) and -independent (nitroglycerin) agonists before and after an intravenous infusion of vehicle or two concentrations of nicotine. Acetylcholine, ADP, and nitroglycerin produced a dose-related dilatation of the cheek pouch arterioles under control conditions. Endothelium-dependent, but not -independent, dilatation of arterioles was modestly impaired by an infusion of a low concentration of nicotine (1.0 μg·kg-1·min-1). Infusion of a higher concentration of nicotine (2 μg·kg-1·min-1), which increased the plasma level of nicotine to 14 ± 1.6 ng/ml, produced a profound selective impairment in endothelium-dependent vasodilatation. We suggest that elevations in plasma nicotine may contribute to the pathogenesis of the peripheral vascular disease observed in smokers.",
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AU - Mayhan, William

AU - Patel, Kaushik P

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N2 - Smoking is a primary risk factor in coronary and peripheral vascular disease. However, the precise component of cigarette smoke that contributes to the pathogenesis of vascular disease remains unclear. The goal of this study was to determine the effect of nicotine on endothelium-dependent dilatation of peripheral resistance arterioles in vivo. We measured the diameter of resistance arterioles (~50 μm in diameter) contained within the microcirculation of the hamster cheek pouch in response to endothelium- dependent (acetylcholine and ADP) and -independent (nitroglycerin) agonists before and after an intravenous infusion of vehicle or two concentrations of nicotine. Acetylcholine, ADP, and nitroglycerin produced a dose-related dilatation of the cheek pouch arterioles under control conditions. Endothelium-dependent, but not -independent, dilatation of arterioles was modestly impaired by an infusion of a low concentration of nicotine (1.0 μg·kg-1·min-1). Infusion of a higher concentration of nicotine (2 μg·kg-1·min-1), which increased the plasma level of nicotine to 14 ± 1.6 ng/ml, produced a profound selective impairment in endothelium-dependent vasodilatation. We suggest that elevations in plasma nicotine may contribute to the pathogenesis of the peripheral vascular disease observed in smokers.

AB - Smoking is a primary risk factor in coronary and peripheral vascular disease. However, the precise component of cigarette smoke that contributes to the pathogenesis of vascular disease remains unclear. The goal of this study was to determine the effect of nicotine on endothelium-dependent dilatation of peripheral resistance arterioles in vivo. We measured the diameter of resistance arterioles (~50 μm in diameter) contained within the microcirculation of the hamster cheek pouch in response to endothelium- dependent (acetylcholine and ADP) and -independent (nitroglycerin) agonists before and after an intravenous infusion of vehicle or two concentrations of nicotine. Acetylcholine, ADP, and nitroglycerin produced a dose-related dilatation of the cheek pouch arterioles under control conditions. Endothelium-dependent, but not -independent, dilatation of arterioles was modestly impaired by an infusion of a low concentration of nicotine (1.0 μg·kg-1·min-1). Infusion of a higher concentration of nicotine (2 μg·kg-1·min-1), which increased the plasma level of nicotine to 14 ± 1.6 ng/ml, produced a profound selective impairment in endothelium-dependent vasodilatation. We suggest that elevations in plasma nicotine may contribute to the pathogenesis of the peripheral vascular disease observed in smokers.

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