TY - JOUR
T1 - Norepinephrine and Epinephrine Release and Adrenergic Mediation of Smoking-Associated Hemodynamic and Metabolic Events
AU - Cryer, Philip E.
AU - Haymond, Morey W.
AU - Santiago, Julio V.
AU - Shah, Suresh D.
PY - 1976/9/9
Y1 - 1976/9/9
N2 - We studied the effects of cigarette smoking, sham smoking and smoking during adrenergic blockade in 10 subjects to determine whether smoking released the sympathetic neurotransmitter norepinephrine, as well as the adrenomedullary hormone epinephrine, and whether smoking-associated hemodynamic and metabolic changes were mediated through adrenergic mechanisms. Smoking-associated increments in mean (S.E.M.) plasma norepinephrine (22723 to 32439 pg per milliliter, P< 0.01) and epinephrine (444 to 11327 pg per milliliter, P< 0.05) were demonstrated. Smoking-associated increments in pulse rate, blood pressure, blood glycerol and blood lactate/pyruvate ratio were prevented by adrenergic blockade; increments in plasma growth hormone and cortisol were not. Since significant smoking-associated increments, in pulse rate, blood pressure and blood lactate/pyruvate ratio, preceded measurable increments in plasma catecholamine concentrations, but were adrenergically mediated, these changes should be attributed to norepinephrine released locally from adrenergic axon terminals within the tissues rather than to increments in circulating catecholamines. (N Engl J Med 295:573-577, 1976). Acute coronary-heart-disease events — acute myocardial infarction or sudden death in patients with coronary-artery disease — are among the disorders strongly associated with cigarette smoking.1Although it has been suggested that smoking may contribute to the development of coronary atherosclerosis per se, several epidemiologic observations suggest the alternative possibility that cigarette smoking triggers acute coronary-heart-disease events in patients with underlying coronary-artery disease. These observations include: Doyle's finding that smoking was a weak independent risk factor but greatly increased the probability of acute coronary events in patients with hypertension or hypercholesterolemia2; the finding that men who were former smokers on.
AB - We studied the effects of cigarette smoking, sham smoking and smoking during adrenergic blockade in 10 subjects to determine whether smoking released the sympathetic neurotransmitter norepinephrine, as well as the adrenomedullary hormone epinephrine, and whether smoking-associated hemodynamic and metabolic changes were mediated through adrenergic mechanisms. Smoking-associated increments in mean (S.E.M.) plasma norepinephrine (22723 to 32439 pg per milliliter, P< 0.01) and epinephrine (444 to 11327 pg per milliliter, P< 0.05) were demonstrated. Smoking-associated increments in pulse rate, blood pressure, blood glycerol and blood lactate/pyruvate ratio were prevented by adrenergic blockade; increments in plasma growth hormone and cortisol were not. Since significant smoking-associated increments, in pulse rate, blood pressure and blood lactate/pyruvate ratio, preceded measurable increments in plasma catecholamine concentrations, but were adrenergically mediated, these changes should be attributed to norepinephrine released locally from adrenergic axon terminals within the tissues rather than to increments in circulating catecholamines. (N Engl J Med 295:573-577, 1976). Acute coronary-heart-disease events — acute myocardial infarction or sudden death in patients with coronary-artery disease — are among the disorders strongly associated with cigarette smoking.1Although it has been suggested that smoking may contribute to the development of coronary atherosclerosis per se, several epidemiologic observations suggest the alternative possibility that cigarette smoking triggers acute coronary-heart-disease events in patients with underlying coronary-artery disease. These observations include: Doyle's finding that smoking was a weak independent risk factor but greatly increased the probability of acute coronary events in patients with hypertension or hypercholesterolemia2; the finding that men who were former smokers on.
UR - http://www.scopus.com/inward/record.url?scp=0017148444&partnerID=8YFLogxK
U2 - 10.1056/NEJM197609092951101
DO - 10.1056/NEJM197609092951101
M3 - Article
C2 - 950972
AN - SCOPUS:0017148444
SN - 0028-4793
VL - 295
SP - 573
EP - 577
JO - New England Journal of Medicine
JF - New England Journal of Medicine
IS - 11
ER -