Related Experiment Video

Updated: Aug 1, 2026

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000
07:46

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000

Published on: October 15, 2010

Deficiency in nitric oxide bioactivity in epicardial coronary arteries of cigarette smokers

K Kugiyama1, H Yasue, M Ohgushi

  • 1Division of Cardiology, Kumamoto University School of Medicine, Japan. kiyo@gpo.kumamoto-u.ac.jp

Journal of the American College of Cardiology
|November 1, 1996
PubMed

Insights

Cigarette smoking impairs nitric oxide's role in regulating coronary artery tone, causing arteries to constrict with acetylcholine and become overly sensitive to nitroglycerin in smokers.

Area of Science:

  • Cardiovascular physiology
  • Endothelial function
  • Vascular pharmacology

Background:

  • Cigarette smoking is a significant risk factor for coronary artery disease.
  • Smoking is common in patients with coronary spastic angina.
  • Long-term smoking suppresses endothelium-dependent arterial relaxation.

Purpose of the Study:

  • To investigate nitric oxide-mediated regulation of epicardial coronary arterial tone in smokers.
  • To compare arterial responses in smokers versus nonsmokers.

Main Methods:

  • Quantitative coronary angiography used to measure epicardial coronary artery diameter.
  • Infusion of acetylcholine and NG-monomethyl-L-arginine (L-NMMA) into the left main coronary artery.
  • Study included 11 current smokers and 17 nonsmokers.

Main Results:

  • Acetylcholine constricted coronary arteries in smokers but dilated them in nonsmokers.
  • L-NMMA abolished acetylcholine-induced dilation in nonsmokers but had minimal effect in smokers.
  • Smokers showed increased dilation to nitroglycerin and impaired nitric oxide bioactivity.

Conclusions:

  • Decreased nitric oxide bioactivity in smokers affects coronary artery tone regulation.
  • Smokers exhibit supersensitivity to acetylcholine's constrictor effects and nitroglycerin's dilator effects.
  • Cigarette smoking significantly alters nitric oxide-mediated control of coronary arteries.
Abstract

More Related Videos

Analytical Techniques for Assaying Nitric Oxide Bioactivity11:28

Analytical Techniques for Assaying Nitric Oxide Bioactivity

Published on: June 18, 2012

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries08:58

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries

Published on: February 25, 2016

Related Concept Videos

Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
Ischemic Heart Disease: Overview01:17

Ischemic Heart Disease: Overview

Ischemic heart disease occurs when the heart's blood supply dwindles, causing an ominous lack of oxygen and nutrients. This deficiency, stemming from reduced or obstructed blood flow, spells danger, leading to heart muscle damage and dysfunction.
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and narrowing...
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
Coronary Artery Disease I: Introduction01:30

Coronary Artery Disease I: Introduction

Coronary Artery Disease (CAD): An Overview with Scientific InsightsCoronary Artery Disease (CAD), often referred to as C-A-D, is a prevalent blood vessel disorder classified under the broader category of atherosclerosis. Atherosclerosis is a pathological process characterized by the hardening and narrowing of arteries due to the accumulation of atherosclerotic plaques. These plaques are composed of cholesterol, fatty substances, inflammatory cells, calcium, and fibrin, reducing blood flow to...
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
Coronary Artery Disease III: Clinical Manifestations01:30

Coronary Artery Disease III: Clinical Manifestations

Coronary Artery Disease (CAD) is a primary health risk worldwide, leading to significant morbidity and mortality. The condition arises from the buildup of atherosclerotic plaques within the coronary arteries, resulting in diminished blood supply to the heart muscle.The clinical manifestations of CAD vary widely, from asymptomatic stages to severe, life-threatening conditions. Understanding these manifestations is crucial for early diagnosis and effective management.Angina Pectoris: The Warning...