Acute and chronic treatment with nicotine impairs reactivity of arterioles in response to activation of potassium channels

William Mayhan, Glenda M. Sharpe

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Although acute and chronic treatment with nicotine impairs nitric oxide synthase-dependent responses of large and small blood vessels, the effect of nicotine on other vasodilator pathways remains uncertain. The goal of the current study was to determine effects of nicotine on dilatation of arterioles to activation of ATP-sensitive potassium channels. Reactivity of cheek pouch arterioles (∼50 μm) was measured during acute (1-2 h) and chronic (2- to 3-week) exposure to nicotine in response to aprikalim, cromakalim, and nitroglycerin. Acute treatment with nicotine impaired dilatation of arterioles in response to aprikalim and cromakalim but not nitroglycerin. Aprikalim and cromakalim (1.0 μM) dilated arterioles by 37 ± 5% and 30 ± 3%, respectively, before, but by only 21 ± 4% and 16 ± 3%, respectively, after infusion of nicotine (p < 0.05). Chronic exposure to nicotine did not alter vasodilatation to nitroglycerin but impaired vasodilatation to aprikalim and cromakalim. In vehicle-treated hamsters, aprikalim and cromakalim (1.0 μM) dilated arterioles by 28 ± 1% and 32 ± 3%, respectively. However, in nicotine-treated hamsters aprikalim and cromakalim (1.0 μM) dilated arterioles by only 3 ± 1% and 13 ± 1%, respectively. Next, the role of superoxide anion in impaired responses of arterioles to aprikalim and cromakalim during acute infusion of nicotine was examined. Treatment with superoxide dismutase attenuated the effects of nicotine on aprikalim and cromakalim. Thus, acute and chronic exposure to nicotine has profound affects on vasodilatation to activation of ATP-sensitive potassium channels, which may be mediated by superoxide anion.

Original languageEnglish (US)
Pages (from-to)695-703
Number of pages9
JournalJournal of Cardiovascular Pharmacology
Volume39
Issue number5
DOIs
StatePublished - May 9 2002

Fingerprint

Potassium Channels
Arterioles
Cromakalim
Nicotine
Nitroglycerin
Vasodilation
KATP Channels
Superoxides
Cricetinae
Dilatation
aprikalim
Cheek
Vasodilator Agents
Nitric Oxide Synthase
Superoxide Dismutase
Blood Vessels

Keywords

  • Aprikalim
  • Arterioles
  • Cheek pouch
  • Cromakalim
  • Endothelium-derived hyperpolarizing factor
  • Hamsters
  • Nitroglycerin

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

Cite this

Acute and chronic treatment with nicotine impairs reactivity of arterioles in response to activation of potassium channels. / Mayhan, William; Sharpe, Glenda M.

In: Journal of Cardiovascular Pharmacology, Vol. 39, No. 5, 09.05.2002, p. 695-703.

Research output: Contribution to journalArticle

@article{a2aeb080a8a84a2e95ddf46e9ab06bfb,
title = "Acute and chronic treatment with nicotine impairs reactivity of arterioles in response to activation of potassium channels",
abstract = "Although acute and chronic treatment with nicotine impairs nitric oxide synthase-dependent responses of large and small blood vessels, the effect of nicotine on other vasodilator pathways remains uncertain. The goal of the current study was to determine effects of nicotine on dilatation of arterioles to activation of ATP-sensitive potassium channels. Reactivity of cheek pouch arterioles (∼50 μm) was measured during acute (1-2 h) and chronic (2- to 3-week) exposure to nicotine in response to aprikalim, cromakalim, and nitroglycerin. Acute treatment with nicotine impaired dilatation of arterioles in response to aprikalim and cromakalim but not nitroglycerin. Aprikalim and cromakalim (1.0 μM) dilated arterioles by 37 ± 5{\%} and 30 ± 3{\%}, respectively, before, but by only 21 ± 4{\%} and 16 ± 3{\%}, respectively, after infusion of nicotine (p < 0.05). Chronic exposure to nicotine did not alter vasodilatation to nitroglycerin but impaired vasodilatation to aprikalim and cromakalim. In vehicle-treated hamsters, aprikalim and cromakalim (1.0 μM) dilated arterioles by 28 ± 1{\%} and 32 ± 3{\%}, respectively. However, in nicotine-treated hamsters aprikalim and cromakalim (1.0 μM) dilated arterioles by only 3 ± 1{\%} and 13 ± 1{\%}, respectively. Next, the role of superoxide anion in impaired responses of arterioles to aprikalim and cromakalim during acute infusion of nicotine was examined. Treatment with superoxide dismutase attenuated the effects of nicotine on aprikalim and cromakalim. Thus, acute and chronic exposure to nicotine has profound affects on vasodilatation to activation of ATP-sensitive potassium channels, which may be mediated by superoxide anion.",
keywords = "Aprikalim, Arterioles, Cheek pouch, Cromakalim, Endothelium-derived hyperpolarizing factor, Hamsters, Nitroglycerin",
author = "William Mayhan and Sharpe, {Glenda M.}",
year = "2002",
month = "5",
day = "9",
doi = "10.1097/00005344-200205000-00010",
language = "English (US)",
volume = "39",
pages = "695--703",
journal = "Journal of Cardiovascular Pharmacology",
issn = "0160-2446",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

TY - JOUR

T1 - Acute and chronic treatment with nicotine impairs reactivity of arterioles in response to activation of potassium channels

AU - Mayhan, William

AU - Sharpe, Glenda M.

PY - 2002/5/9

Y1 - 2002/5/9

N2 - Although acute and chronic treatment with nicotine impairs nitric oxide synthase-dependent responses of large and small blood vessels, the effect of nicotine on other vasodilator pathways remains uncertain. The goal of the current study was to determine effects of nicotine on dilatation of arterioles to activation of ATP-sensitive potassium channels. Reactivity of cheek pouch arterioles (∼50 μm) was measured during acute (1-2 h) and chronic (2- to 3-week) exposure to nicotine in response to aprikalim, cromakalim, and nitroglycerin. Acute treatment with nicotine impaired dilatation of arterioles in response to aprikalim and cromakalim but not nitroglycerin. Aprikalim and cromakalim (1.0 μM) dilated arterioles by 37 ± 5% and 30 ± 3%, respectively, before, but by only 21 ± 4% and 16 ± 3%, respectively, after infusion of nicotine (p < 0.05). Chronic exposure to nicotine did not alter vasodilatation to nitroglycerin but impaired vasodilatation to aprikalim and cromakalim. In vehicle-treated hamsters, aprikalim and cromakalim (1.0 μM) dilated arterioles by 28 ± 1% and 32 ± 3%, respectively. However, in nicotine-treated hamsters aprikalim and cromakalim (1.0 μM) dilated arterioles by only 3 ± 1% and 13 ± 1%, respectively. Next, the role of superoxide anion in impaired responses of arterioles to aprikalim and cromakalim during acute infusion of nicotine was examined. Treatment with superoxide dismutase attenuated the effects of nicotine on aprikalim and cromakalim. Thus, acute and chronic exposure to nicotine has profound affects on vasodilatation to activation of ATP-sensitive potassium channels, which may be mediated by superoxide anion.

AB - Although acute and chronic treatment with nicotine impairs nitric oxide synthase-dependent responses of large and small blood vessels, the effect of nicotine on other vasodilator pathways remains uncertain. The goal of the current study was to determine effects of nicotine on dilatation of arterioles to activation of ATP-sensitive potassium channels. Reactivity of cheek pouch arterioles (∼50 μm) was measured during acute (1-2 h) and chronic (2- to 3-week) exposure to nicotine in response to aprikalim, cromakalim, and nitroglycerin. Acute treatment with nicotine impaired dilatation of arterioles in response to aprikalim and cromakalim but not nitroglycerin. Aprikalim and cromakalim (1.0 μM) dilated arterioles by 37 ± 5% and 30 ± 3%, respectively, before, but by only 21 ± 4% and 16 ± 3%, respectively, after infusion of nicotine (p < 0.05). Chronic exposure to nicotine did not alter vasodilatation to nitroglycerin but impaired vasodilatation to aprikalim and cromakalim. In vehicle-treated hamsters, aprikalim and cromakalim (1.0 μM) dilated arterioles by 28 ± 1% and 32 ± 3%, respectively. However, in nicotine-treated hamsters aprikalim and cromakalim (1.0 μM) dilated arterioles by only 3 ± 1% and 13 ± 1%, respectively. Next, the role of superoxide anion in impaired responses of arterioles to aprikalim and cromakalim during acute infusion of nicotine was examined. Treatment with superoxide dismutase attenuated the effects of nicotine on aprikalim and cromakalim. Thus, acute and chronic exposure to nicotine has profound affects on vasodilatation to activation of ATP-sensitive potassium channels, which may be mediated by superoxide anion.

KW - Aprikalim

KW - Arterioles

KW - Cheek pouch

KW - Cromakalim

KW - Endothelium-derived hyperpolarizing factor

KW - Hamsters

KW - Nitroglycerin

UR - http://www.scopus.com/inward/record.url?scp=0036240330&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036240330&partnerID=8YFLogxK

U2 - 10.1097/00005344-200205000-00010

DO - 10.1097/00005344-200205000-00010

M3 - Article

VL - 39

SP - 695

EP - 703

JO - Journal of Cardiovascular Pharmacology

JF - Journal of Cardiovascular Pharmacology

SN - 0160-2446

IS - 5

ER -