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Cited by 106Receptor Mechanisms and SignalingStress Responses and CortisolNeuroscience and Neuropharmacology Research

Peripheral and Central Effects of Circulating Catecholamines

Open access
William Tank, A., Lee Wong, Dona·2015·Comprehensive Physiology
DOI 10.1002/j.2040-4603.2015.tb00599.x
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Abstract

Physical challenges, emotional arousal, increased physical activity, or changes in the environment can evoke stress, requiring altered activity of visceral organs, glands, and smooth muscles. These alterations are necessary for the organism to function appropriately under these abnormal conditions and to restore homeostasis. These changes in activity comprise the “fight‐or‐flight” response and must occur rapidly or the organism may not survive. The rapid responses are mediated primarily via the catecholamines, epinephrine, and norepinephrine, secreted from the adrenal medulla. The catecholamine neurohormones interact with adrenergic receptors present on cell membranes of all visceral organs and smooth muscles, leading to activation of signaling pathways and consequent alterations in organ function and smooth muscle tone. During the “fight‐or‐flight response,” the rise in circulating epinephrine and norepinephrine from the adrenal medulla and norepinephrine secreted from sympathetic nerve terminals cause increased blood pressure and cardiac output, relaxation of bronchial, intestinal and many other smooth muscles, mydriasis, and metabolic changes that increase levels of blood glucose and free fatty acids. Circulating catecholamines can also alter memory via effects on afferent sensory nerves impacting central nervous system function. While these rapid responses may be necessary for survival, sustained elevation of circulating catecholamines for prolonged periods of time can also produce pathological conditions, such as cardiac hypertrophy and heart failure, hypertension, and posttraumatic stress disorder. In this review, we discuss the present knowledge of the effects of circulating catecholamines on peripheral organs and tissues, as well as on memory in the brain. © 2015 American Physiological Society. Compr Physiol 5:1‐15, 2015.

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Crossref · 10.1002/j.2040-4603.2015.tb00599.x

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  • Lipolysis is largely controlled via the endocrine system.

    “The process of lipolysis is largely controlled via the endocrine system [12].”

    From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [12]

    The “Metabolic effects” section says circulating catecholamines activate triglyceride lipase in adipocytes, supporting endocrine regulation of lipolysis. It does not establish that the endocrine system largely controls lipolysis; the review also describes effects of norepinephrine released directly at synapses. Page numbers are unavailable in our copy. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • Training status affects catecholamine release and receptor sensitivity, endogenous substrate concentrations, and cellular transport protein expression; all contribute to the variability of when MFO occurs relative to exercise intensity.

    “Training status has been shown to effect catecholamine release and receptor sensitivity [12], endogenous substrate concentrations, and cellular transport protein expression; all of which contribute to the variability of when MFO occurs relevant to exercise intensity [1].”

    From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [12]

    The Conclusion (page unavailable) says circulating catecholamines rise during increased physical activity and that sustained elevations can cause receptor desensitization. It does not say that training status affects catecholamine release or receptor sensitivity. The later claims about substrates, transport proteins, and MFO are attached to a different citation in the printed sentence. (LLM, conf=0.76)

    Experimental — accuracy not yet measured

  • As exercise intensity increases, catecholamine concentrations increase, facilitating a concurrent increase of serum CHO and FAs into the blood.

    “As exercise intensity increases, so does catecholamine concentrations facilitating a concurrent increase of serum CHO and FAs into the blood [12].”

    From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [12]

    The Conclusion says circulating catecholamines increase during enhanced physical activity, and “Metabolic effects” says epinephrine raises blood glucose and free fatty acids. The copy does not establish that catecholamine concentrations rise progressively with exercise intensity, or that both substrates increase concurrently as intensity rises. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Increased epinephrine concentrations that parallel increases in exercise intensity stimulate both glycogenolysis and gluconeogenesis.

    “Increased epinephrine concentrations that parallel increases in exercise intensity stimulate both glycogenolysis and gluconeogenesis [12].”

    From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [12]

    The Metabolic effects section says circulating epinephrine activates glycogenolysis. The Epinephrine and norepinephrine section says exercise increases epinephrine secretion, but our copy does not establish that concentrations track exercise intensity or that epinephrine stimulates gluconeogenesis. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • The hormonal mechanisms that stimulate lipid metabolism are based primarily on catecholamines, cortisol, growth hormone, where insulin is inhibitory.

    “The hormonal mechanisms that stimulate lipid metabolism are based primarily on catecholamines [12], cortisol, growth hormone, where insulin is inhibitory [16].”

    From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [12]

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Research works printed but not linked: 1

  1. [110]110. Selye H. The Stress of Life. New York: McGraw Hill, 1975.

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Authors
William Tank, A., & Lee Wong, D.
Affiliations
  • Department of Pharmacology & Physiology University of Rochester Medical Center Rochester NY USA
  • Department of Psychiatry Harvard Medical School, McLean Hospital Belmont MA USA
Venue
Comprehensive Physiology
Publisher
Wiley
Published
2015-01
Volume
5
Issue
1
Pages
1-15
ISSN
2040-4603 (ISSN-L)
DOI
10.1002/j.2040-4603.2015.tb00599.x
OpenAlex
W4409092676
Cited by
106
References
134
Citations by year
2026: 23 · 2025: 32 · 2024: 4 · 2023: 3 · 2022: 2 · 2021: 4 · 2020: 3 · 2018: 9 · 2017: 12 · 2016: 12 · 2015: 2
FWCI
5.06
Type
journal article
Language
en
Open access
Licence
Locations
Comprehensive physiology (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
circulating catecholamines, epinephrine, norepinephrine, fight-or-flight response, stress response, adrenergic receptors, smooth muscle relaxation, blood pressure, cardiac output, memory, cardiac hypertrophy, heart failure, hypertension, post-traumatic stress disorder, adrenal medulla, sympathetic nerve terminals

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