Effect of cigarette smoke extract on arteriolar dilatation in vivo

Abstract

The goal of this study was to determine whether cigarette smoke extract alters dilatation of arterioles in vivo in response to agonists that produce activation of ATP-sensitive potassium channels and activation of adenylate cyclase. By using intravital microscopy, we measured diameter of arterioles contained within the microcirculation of the hamster cheek pouch during suffusion with agonists in the absence and presence of cigarette smoke extract (0.1, 0.5, and 1.0%). Before treatment with cigarette smoke extract, activation of ATP-sensitive potassium channels with aprikalim and cromakalim produced dose-related dilatation of cheek pouch arterioles. Similarly, activation of adenylate cyclase with isoproterenol and forskolin produced dose-related dilatation of cheek pouch arterioles before treatment with cigarette smoke extract. Superfusion of 0.1% cigarette smoke extract did not change baseline diameter of arterioles and did not alter responses of cheek pouch arterioles to activation of ATP-sensitive potassium channels and adenylate cyclase. Superfusion of 0.5 and 1.0% cigarette smoke extract also did not alter baseline diameter of arterioles but did impair dilatation of arterioles in response to activation of ATP-sensitive potassium channels and adenylate cyclase. These findings suggest that cigarette smoke extract impairs dilatation of resistance arterioles in response to activation of important cellular dilator pathways.

SASH1, a new potential link between smoking and atherosclerosis

“…It is therefore considered to be atheroprotective. Both active and passive smokers show decreased vasodilatation [52][53][54] , which corroborates many studies that have shown that cigarette smoke is associated with decreased NO availability 54,69 . Several studies investigated the molecular pathways leading to decreased NO availability in smokers.…”

“…In the case of atherosclerosis, it has been demonstrated that intimal-medial thickness, a routine measurement to determine the advancement of atherosclerosis, is increased in both passive and active smokers 51 . Furthermore, both active and passive smoking are associated with decreased vasodilatation in various vascular beds (in different sites in the arteries) 52,53,54 . Finally, cigarette smoking significantly increases, LDL levels 55 , lipid oxidation, leukocyte counts and inflammatory markers in humans 56,57,58 (see section I.3.b), all of these processes being known to favor plaque growth.…”

Fetal and Neonatal Nicotine Exposure Differentially Regulates Vascular Contractility in Adult Male and Female Offspring

“…Nicotine can contribute to the development of cardiovascular disorders through a variety of mechanisms. It has been shown that the most significant effects of nicotine are through its influence on the vascular tone (Mayhan and Sharpe, 1996;Wang and Wang, 2000), the hemostatic system (Powell, 1998), and the endothelium (Mayhan et al, 1999). The combination of these effects leads to the development of various cardiovascular disorders such as atherosclerosis, cardiac arrhythmias, coronary artery disease, and hypertension.…”

Troponin I level in risk stratification of non-ST-elevation myocardial infarction in smokers

“…Several studies have reported that cigarette smoking exposes individual to cardiovascular morbidity and mortality (Mayhan and Sharpe, 1996). Troponin I is considered as valuable biomarker to convey prognostic information for patient with non ST-elevation myocardial infarction.…”

“…Cigarette smoking is one of the most important risk factors for acute coronary syndrome. Smoking impacts all the phases of atherosclerosis (Mayhan and Sharpe, 1996). In Bangladesh over 50% male and 3% female are cigarette smokers (Millat, 2005).…”