Cited by 1,101Smoking Behavior and CessationBlood Pressure and Hypertension StudiesReceptor Mechanisms and Signaling

Norepinephrine and Epinephrine Release and Adrenergic Mediation of Smoking-Associated Hemodynamic and Metabolic Events

Cryer, Philip E., Haymond, Morey W., Santiago, Julio V., Shah, Suresh D.·1976·New England Journal of Medicine

Abstract

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 (227 +/- 23 to 324 +/- 39 pg per milliliter, P less than 0.01) and epinephrine (44 +/- to 113 +/- 27 pg per milliliter, P less than 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.

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Registry

Crossref · 10.1056/nejm197609092951101

Cites

29 of 29 references verified0 citation errors · 0 not checkable

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  • Mean plasma epinephrine concentrations rise nearly 2-fold during quiet standing, ~3-fold during cigarette smoking, from 2-13-fold during mild to heavy exercise, and 50-fold during insulin-induced hypoglycemia.

    “mean plasma epinephrine concentrations rise nearly 2-fold during quiet standing (6), ~3-fold during cigarette smoking (26), from 2–13-fold during mild to heavy exercise (27), and 50fold during insulin-induced hypoglycemia (28).”

Cites

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Research works printed but not linked: 3

  1. Raab, 1943, Exp Med Surg, 1, 402
  2. Karl, 1972, J Lab Clin Med, 80, 434
  3. Snedecor GW: Statistical Methods. Fifth edition. Ames, Iowa, Iowa State College Press, 1956

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Authors
Cryer, P. E., Haymond, M. W., Santiago, J. V., & Shah, S. D.
Affiliations
Washington University in St. Louis (US)
Venue
New England Journal of Medicine
Published
1976-09-09
Volume
295
Issue
11
Pages
573-577
ISSN
  • 0028-4793 (ISSN-L)
  • 1533-4406
OpenAlex
W2341712066
Cited by
1,101
References
29
Citations by year
2026: 6 · 2025: 6 · 2024: 10 · 2023: 14 · 2022: 18 · 2021: 19 · 2020: 22 · 2019: 20 · 2018: 14 · 2017: 22 · 2016: 24 · 2015: 13 · 2014: 23 · 2013: 15 · 2012: 19
FWCI
19.23
Type
journal article
Language
en
Open access
closed
Locations
  • New England Journal of Medicine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
Keywords
cigarette smoking, norepinephrine, epinephrine, sympathetic nervous system, adrenergic blockade, plasma catecholamines, hemodynamic response, blood pressure, pulse rate, blood lactate, growth hormone, cortisol, adrenergic neurotransmission
MeSH terms
Adult, Blood Pressure, Epinephrine, Glycerol, Hemodynamics, Humans, Hydrocortisone, Lactates, Male, Norepinephrine, Phentolamine, Propranolol, Pulse, Pyruvates, Smoking, Growth Hormone, Sympathetic Nervous System, Sympatholytics

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