All About Catecholamines in the Stress Response

Catecholamine and cortisol reaction to childbirth

All About Catecholamines in the Stress Response

  1. Åkerstedt, T. (1979). Altered sleep/wake patterns and circadian rhythms. Laboratory and field studies of sympathomedullary and related variables. Acta Physiological Scandinavica, Suppl. 469, 1–48.

  2. Bergant, A. M., Kirchler, H., Heim, K., Daxenbichler, G., Herold, M., & Schröcksnadel, H. (1998). Childbirth as a biological model for stress? Gynecologic and Obstetric Investigation, 45, 181–185.

    • PubMed
    • Article
    • Google Scholar
  3. Bordens, K. S., & Abbott, B. B. (1988). Research design and methods: A process approach. Mountain View, CA: Mayfield.

  4. Chan, E. C., Smith, R., Lewin, T., Brinsmead, M. W., Zhang, H. P., Cubis, J., Thornton, K., & Hurt, D. (1993). Plasma corticotropin-releasing hormone, β-endorphin and cortisol inter-relationships during human pregnancy. Acta Endocrinologica, 128, 339–344.

  5. Chestnut, D., & Gibbs, C. (1991). Obstetrics anesthesia. In S. Gabbe, J. Nebyl, & J. L. Simpson (Eds.), Obstetrics: Normal and problem pregnancies (pp. 493–539). New York: Churchill Livingstone.

  6. Frankenhaeuser, M. (1991). The psychophysiology of sex differences as related to occupational status. In M. Frankenhaeuser, U. Lundberg, & M. Chesney (Eds.), Women, work and health: Stress and opportunities (pp. 39–64). New York: Plenum.

  7. Frankenhaeuser, M., & Lundberg, U. (1985). Sympathetic-adrenal and pituitary-adrenal responses to challenge. In P. Pichot, R. Berner, S. Wolf, & K. Thau (Eds.), Psychiatry (Vol. 2, pp. 699–704). London: Plenum.

  8. Haeckel, R., & Bucklitsch, I. (1987). The comparability ofethanol concentrationinperipheral blood and saliva. The phenomena of variation in saliva to blood concentration ratio. Journal of Clinical Biochemistry, 25, 199–204.

  9. Hjemdahl, P., Larsson, P. T., Bradley, T., Åkerstedt, T., Anderzén, I., Sigurdssson, K., Gillberg, M., & Lundberg, U. (1989). Catecholamine measurements in urine high-performance liquid chromatography with amperometric detection—Comparison with anautoanalyser fluorescence method. Journal of Chromatography, 494, 53–66.

    • PubMed
    • Article
    • Google Scholar
  10. Jouppila, R., Puolakka, J., Kauppila, A., & Vuori, J. (1984). Maternal and umbilical cord plasma noradrenaline concentrations during labour with and without segmental extradural analgesia, and during caesarean section. British Journal of Anaesthesia, 56, 251–255.

    • PubMed
    • Article
    • Google Scholar
  11. Kirschbaum, C., & Hellhammer, D. H. (1989). Salivary cortisol in psychobiological research: An overview. Neuropsychobiology, 22, 150–169.

    • PubMed
    • Article
    • Google Scholar
  12. Lagercrantz, H., & Slotkin, T. A. (1985). The “stress” of being born. American Scientist, 12, 100–110.

  13. Lederman, E., Lederman, R. P., Work, B. A., & McCann, D. S. (1977). Endogenous plasma epinephrine and norepinephrine in last-trimester pregnancy and labor. American Journal of Obstetrics and Gynecology, 1, 5–8.

  14. Lederman, E., Lederman, R. P., Work, B. A., & McCann, D. S. (1978). The relationship of maternal anxiety, plasma catecholamines, and plasma cortisol to progress in labor. American Journal of Obstetrics and Gynecology, 5, 495–500.

  15. Lederman, R. P., Lederman, E., Work, B. A., & McCann, D. S. (1985). Anxiety and epinephrine in multiparous women in labor: Relationshipto duration of labor and fetal heart rate pattern. American Journal of Obstetrics and Gynecology, 8, 870–877.

  16. Lovallo, W. R., & Thomas, T. L. (1989). Stress hormones in psychophysiological research: Emotional, behavioral, and cognitive implications. In J. T. Cacioppo, L. G. Tassinary, & G. Berntson (Eds.), Handbook of psychophysiology (pp. 12–33). New York: Cambridge University Press.

  17. Lundberg, U. (2000). Catecholamines. In G. Fink (Eds.), Encyclopedia of stress (pp. 408–413). San Diego, CA: Academic.

  18. Lundberg, U., Holmberg, L., & Frankenhaeuser, M. (1988). Urinary catecholamines: Comparison between HPLC with electrochemical detection and fluorophotometric assay. Pharmacology, Biochemistry & Behavior, 31, 287–289.

  19. Lundberg, U., & Johansson, G. (2000). Stress and health risks in repetitive work and supervisory monitoring work. In R. Backs & W. Boucsein (Eds.), Engineering psychophysiology: Issues and applications (pp. 339–359). Mahwah, NJ: Lawrence Erlbaum Associates, Inc.

  20. McEwen, B. S. (1998). Protective and damaging effects of stress mediators. New England Journal of Medicine, 338, 171–179.

    • PubMed
    • Article
    • Google Scholar
  21. Ohana, E., Mazor, M., Chaim, W., Levy, J., Sharoni, Y., Leiberman, J. R., & Glezerman, M. (1996). Maternal plasma and amniotic fluid cortisol and progesterone concentrations between women with and without term labor. Journal of Reproductive Medicine, 2, 80–86.

  22. Riggin, R. M., & Kissinger, P. T. (1977). Determination of catecholamines in urine by reverse-phase liquid chromatography with electrochemical detection. Analytical Chemistry, 49, 2109–2111.

    • PubMed
    • Article
    • Google Scholar
  23. Salmon, P., & Drew, N. C. (1992). Multidimensional assessment of women’s experience of childbirth: Relationship to obstetric procedure, antenatal preparation and obstetric history. Journal of Psychosomatic Research, 36, 317–327.

    • PubMed
    • Article
    • Google Scholar
  24. Shnider, S. M., Abboud, T. K., Artal, R., Henriksen, E. H., Stefani, S. J., & Levinson, G. (1983). Maternal catecholamines decrease during labor after lumbar epidural anesthesia. American Journal of Obstetrics and Gynecology, 1, 13–15.

  25. Simkin, P. (1986). Stress, pain and catecholamines in labor: Part 1. A review. Birth, 13, 227–233.

    • PubMed
    • Article
    • Google Scholar
  26. Smith, R., Cubis, J., Brinsmead, M., Lewin, T., Singh, B., Owens, P., Chan, E. C., Hall, C. S., Adler, R., Lovelock, M., Hurt, D., Rowley, M., & Nolan, M. (1990). Mood changes, obstetric experience and alterations in plasma cortisol, beta-endorphin and corticotrophin releasing hormone during pregnancy and the puerperium. Journal of Psychosomatic Research, 34, 53–69.

    • PubMed
    • Article
    • Google Scholar
  27. Tinkanen, H., Rorarius, M., & Metsä-Ketelä, T. (1993). Catecholamine concentrations in venous plasma and cerebrospinal fluid in normal and complicated pregnancy. Gynecologic and Obstetric Investigation, 35, 7–11.

    • PubMed
    • Article
    • Google Scholar
  28. Waldenström, U., Borg, I-M., Olsson, B., Sköld, M., & Wall, S. (1996). The childbirth experience: A study of 295 new mothers. Birth, 23, 144–153.

    • PubMed
    • Article
    • Google Scholar

Source: https://link.springer.com/article/10.1207/S15327558IJBM0801_04

The 3 Major Stress Hormones, Explained

All About Catecholamines in the Stress Response

Thanks to the work of our sympathetic nervous system, the “fight or flight” system that takes over when we're stressed, when you see your boss's name in your inbox late at night, your body reacts there's a lion on the loose.

Behind the wide range of both physical and mental reactions to stress are a number of hormones that are in charge of adding fuel to the fire.

Adrenaline
What It Is: Commonly known as the fight or flight hormone, it is produced by the adrenal glands after receiving a message from the brain that a stressful situation has presented itself.

What It Does: Adrenaline, along with norepinephrine (more on that below), is largely responsible for the immediate reactions we feel when stressed. Imagine you're trying to change lanes in your car, says Amit Sood, M.D.

, director of research at the Complementary and Integrative Medicine and chair of Mayo Mind Body Initiative at Mayo Clinic. Suddenly, from your blind spot, comes a car racing at 100 miles per hour. You return to your original lane and your heart is pounding.

Your muscles are tense, you're breathing faster, you may start sweating. That's adrenaline.

Along with the increase in heart rate, adrenaline also gives you a surge of energy — which you might need to run away from a dangerous situation — and also focuses your attention.

Norepinephrine
What It Is: A hormone similar to adrenaline, released from the adrenal glands and also from the brain, says Sood.

What It Does: The primary role of norepinephrine, adrenaline, is arousal, says Sood. “When you are stressed, you become more aware, awake, focused,” he says.

“You are just generally more responsive.

” It also helps to shift blood flow away from areas where it might not be so crucial, the skin, and toward more essential areas at the time, the muscles, so you can flee the stressful scene.

Although norepinephrine might seem redundant given adrenaline (which is also sometimes called epinephrine), Sood imagines we have both hormones as a type of backup system. “Say your adrenal glands are not working well,” he says. “I still want something to save me from acute catastrophe.”

Depending on the long-term impact of whatever's stressing you out — and how you personally handle stress — it could take anywhere from half an hour to a couple of days to return to your normal resting state, says Sood.

Cortisol
What It Is: A steroid hormone, commonly known as the stress hormone, produced by the adrenal glands.

What It Does: It takes a little more time — minutes, rather than seconds — for you to feel the effects of cortisol in the face of stress, says Sood, because the release of this hormone takes a multi-step process involving two additional minor hormones.

First, the part of the brain called the amygdala has to recognize a threat. It then sends a message to the part of the brain called the hypothalamus, which releases corticotropin-releasing hormone (CRH). CRH then tells the pituitary gland to release adrenocorticotropic hormone (ACTH), which tells the adrenal glands to produce cortisol. Whew!

In survival mode, the optimal amounts of cortisol can be life saving. It helps to maintain fluid balance and blood pressure, says Sood, while regulating some body functions that aren't crucial in the moment, reproductive drive, immunity, digestion and growth.

But when you stew on a problem, the body continuously releases cortisol, and chronic elevated levels can lead to serious issues. Too much cortisol can suppress the immune system, increase blood pressure and sugar, decrease libido, produce acne, contribute to obesity and more.

“Ducks walk a lake, flap their wings and they fly off,” says Sood. “When you face something stressful, particularly if it's not ly to repeat or doesn't have a huge long-term impact, you want to be able to shake it off and move on with life.”

Of course, he adds, estrogen and testosterone are also hormones that affect how we react to stress, as are the neurotransmitters dopamine and serotonin. But the classic fight-or-flight reaction is mostly due to the three major players mentioned above. How do you react to stress? Let us know in the comments.

Source: https://www.huffpost.com/entry/adrenaline-cortisol-stress-hormones_n_3112800

Epinephrine vs. norepinephrine: Differences, functions, and high levels

All About Catecholamines in the Stress Response

Epinephrine and norepinephrine belong to a group of compounds called catecholamines, and they act as both neurotransmitters and hormones. While these compounds have similar chemical structures, they produce different effects on the body.

Epinephrine is also known as adrenaline, while some people refer to norepinephrine as noradrenaline. Both of these substances play a role in the regulation of the sympathetic nervous system, which is the part of the autonomic nervous system that is responsible for the body’s “fight or flight” response.

In this article, we discuss the similarities and differences between epinephrine and norepinephrine, along with their functions. We also cover their medical uses and the health effects of having too much or too little of either compound in the body.

Share on PinterestEpinephrine and norepinephrine both play a role in the body’s “fight-or-flight” response.

Epinephrine and norepinephrine are both hormones and neurotransmitters.

Hormones are chemical messengers that travel through the bloodstream. The endocrine glands and reproductive organs make and secrete a wide range of hormones to regulate the body’s organs, tissues, and cells.

Neurotransmitters are also a type of chemical messenger, but they only occur in nerve cells and travel across synapses, which are junctions where two nerve fibers meet. Nerves cells produce neurotransmitters in response to electrical impulses.

The adrenal medulla, the inner portion of the adrenal gland, regulates and secretes both epinephrine and norepinephrine in response to stress and other imbalances in the body, such as low blood pressure.

Epinephrine activates both alpha- and beta-adrenoreceptors in cells, whereas norepinephrine mainly stimulates alpha-adrenoreceptors.

We discuss the main functions of epinephrine and norepinephrine below:

Epinephrine

When the brain perceives danger, the amygdala triggers the hypothalamus to activate the autonomic nervous system.

Signals from the autonomic nervous system stimulate the adrenal gland to start pumping epinephrine into the bloodstream. People often refer to this surge of epinephrine as an adrenaline rush or the fight or flight response.

Epinephrine affects the heart, lungs, muscles, and blood vessels. Its release into the bloodstream brings about several physiological changes, such as:

  • increased heart rate and blood flow
  • faster breathing
  • raised blood sugar levels
  • increased strength and physical performance

Norepinephrine

The adrenal medulla produces norepinephrine in response to low blood pressure and stress. Norepinephrine promotes vasoconstriction, which is a narrowing of the blood vessels, and this increases blood pressure.

epinephrine, norepinephrine also increases the heart rate and blood sugar levels.

Chronic stress, poor nutrition, some medications, and certain health conditions can affect the body’s ability to produce or respond to epinephrine and norepinephrine.

A rare condition called genetic dopamine beta-hydroxylase deficiency prevents the body from converting dopamine into norepinephrine.

According to a 2018 article, genetic dopamine beta-hydroxylase deficiency results from a mutation in the norepinephrine transporter gene g237c. The authors concluded that this condition might decrease sympathetic nerve activity and increase the risk of damage to the heart and blood vessels.

Low levels of epinephrine and norepinephrine can result in physical and mental symptoms, such as:

In addition, norepinephrine plays a role in focus and promotes periods of sustained attention. Low levels of norepinephrine may contribute to the development of attention deficit hyperactivity disorder (ADHD).

The following medications can increase levels of norepinephrine:

  • amphetamines, such as methylphenidate (Ritalin) and dextroamphetamine (Adderall)
  • serotonin-norepinephrine reuptake inhibitors (SNRIs), such as venlafaxine (Effexor) and duloxetine (Cymbalta)

Share on PinterestHaving high levels of epinephrine or norepinephrine can cause high blood pressure.

Certain medical conditions, such as tumors, chronic stress, and obesity, can affect the adrenal glands and cause excess production of epinephrine and norepinephrine.

Symptoms of high levels of epinephrine or norepinephrine can include:

A 2018 research paper states that having high levels of norepinephrine can increase a person’s risk of cardiovascular and kidney damage.

An epinephrine overdose can occur in people who use epinephrine injections to treat certain medical conditions. An overdose of injected epinephrine can lead to dangerously high blood pressure, stroke, or even death.

Synthetic forms of epinephrine and norepinephrine have several medical uses, which we discuss below:

Neuropeptide–Catecholamine Interactions in Stress

All About Catecholamines in the Stress Response
Author information Copyright and License information Disclaimer

Neuropeptides and catecholamines act as neurotransmitters within circuits of the central and peripheral nervous systems that mediate both systemic and psychological stress responses, as well as long-term adaptation and maladaptation to stress recognizable clinically as survival with resilience, or survival with cost, as manifested in anxiety, depression, PTSD, and other human behavioral disorders. The interactions between catecholamines and neuropeptides within some of these circuits are summarized in this chapter and described in detail in the three chapters following.

It has long been appreciated that central nervous system (CNS) noradrenergic systems set the tone for organismic response to stress, in particular at the level of the locus coeruleus (LC) and its projections to limbic cortex, extended amygdala, and hypothalamus.

Noradrenergic neurons also mediate the autonomic effector limb of the stress response, via increased heart rate and peripheral vascular resistance, and visceral organ activation. Epinephrine release from the adrenal medulla constitutes the very hallmark of acute stress responses.

Between the perception of threat and the autonomic response to it, a complex intervening circuitry sets the sensitivity and gain of the stress response. Neuropeptides are employed as transmitters in this circuitry. There is a growing understanding of opiate peptide effects on arousal and hedonic tone.

Pituitary adenylate cyclase-activating polypeptide (PACAP) has been discovered to be a critical neurotransmitter mediating activation of the hypothalamic–pituitary adrenal (HPA) and hormonal sympathetic adrenal (HSA) axes by stress.

Corticotropin-releasing hormone (CRH) not only initiates HPA activation via release of adrenocorticotropic hormone (ACTH) from the pituitary but also is released from hypothalamic and extrahypothalamic neurons to feed back on noradrenergic systems driving central to peripheral stress “executive” programs.

Striking new findings in the last decade or so have accelerated progress in understanding how, where, and when neuropeptide–catecholamine interactions occur in brain and periphery.

A new picture of stress circuitry has emerged, in which catecholamine and neuropeptide systems are intimately intercalated, both centrally and peripherally, during response to both systemic and psychogenic stress. This neurochemical and anatomical integration allows responses to acute stressors to be translated into long-term changes. These can be both adaptive, and maladaptive, for modern individuals experiencing a range of stressors perceived as threats to homeostasis by limbic and hypothalamic circuits whose final output is activation of the HPA and HSA axes, or the sympathetic nervous system (SNS).

Several contributions to this volume describe recent advances in our understanding of the final output systems shown in Fig. 18.1, that is, how adrenal cortex, adrenal medulla, and postganglionic sympathetic neurons effect acute stress responses and adaptively transduce chronic stress responses.

The CNS circuits mediating acute and chronic stress responses, however, are not above the fray after causing the activation of the axes depicted in Fig. 18.1 (and see Stroth et al., 2011).

Rather, the brain is itself affected by peripherally generated glucocorticoids, and catecholamine-dependent metabolic changes occurring in acute and chronic stress.

A clear indication of this is adaptive and maladaptive behaviors associated with chronic psychological stress that include depression, overeating, sleep disturbance, and immune dysregulation and, in perhaps, the most clinically dramatic fashion, posttraumatic stress disorder (PTSD).

The contributions to this volume on neuropeptide–catecholamine interactions in stress, following on this overview, sum up to an overarching picture of catecholamine–neuropeptide systems that are “sandwiched” between the arousal response conveyed from the sensorium to the brain in large part via the noradrenergic system of the LC, and the final effector system shown in Fig. 18.1, a hybrid catecholamine/corticosteroid hormone output. In Chapter 21, Tomris Mustafa summarizes the role of PACAP as a neuropeptide important in modulating the stress response at several levels. First, PACAP is released from the splanchnic nerve during both acute and chronic stress, whether systemic/physical (hypoglycemia, cold, sepsis) or psychogenic/psychological (restrain/immobilization, social defeat) to allow catecholamine release. Second, PACAP controls activation of the HPA axis at a central level, but this level of control is operative for psychogenic stress only, and not for the systemic stress response.

This control appears to be exerted primarily at the level of activation of CRH neurons in the paraventricular hypothalamus.

In Chapter 20, Watts and Kahn elegantly describe the fully complementary regulation of CRH during systemic—but not psychogenic—stress by noradrenergic inputs (presumably arising mainly from A1/A2 noradrenergic brain stem cell groups— see Itoi et al. in Chapter 8 of this volume).

This regulation is ly mediated by precise ERK-dependent control of both CRH synthesis and CRH secretion into the portal circulation—the actual final effector for pituitary ACTH release and subsequent hormonal secretion of corticosterone/cortisol.

The LC, in addition to mediating the gain of the initial stress response, is “carbon-copied” on activation of CRH neurons by feedback from projections from the amygdala, as well as potentially from the PVN, back to the LC, as outlined by Van Bockstaele and Valentino in Chapter 19 of this volume.

Multiple other opiopeptidergic inputs to LC from limbic stations (dynorphin), and via corelease with other transmitters from the PGi, the pathway through which LC is first activated by sensory cues/stimuli (enkephalin) may be the substrates through which opiate peptide agonists and antagonists, and CRH antagonists, can exert marked effects on stress-dependent anhedonia, depression, and cognitive dysfunction.

Catecholamine neurotransmitters and neuropeptides both interact with GPCRs and are released from large dense-cored vesicles (and in some cases from tubulovesicular structures, e.g.

, dopamine release in substantia nigra) in response to high-frequency or burst neuronal firing of the type associated with the conduction of stress signaling in the CNS and peripheral nervous system.

Ultimately, the stress response requires a sensory input, or a representation of a threat to the conscious brain, to trigger convergence on the hypothalamus leading to AHS/SNS and HPA activation. Activation of CNS circuits to complete this loop requires a “stressed brain” and one that is furthermore additionally acted upon by the stress hormones released peripherally (Fig.

18.2). In some cases, processing of threat responses by the brain may transition it from a homeostatically to an allostatically responding organ, with pathophysiological consequences (PTSD, depression, anxiety) as suggested by McEwen (2008).

Integration of the new neurochemical, neurophysiological, and neuroanatomical facts put forward about catecholamine–neuropeptide interactions in the contributions following should help provide translationally relevant answers to two major questions about the neurochemistry and neuropharmacology of stress responses.

The first is how are catecholaminergic–peptidergic circuit interactions patterned in brainstem, hypothalamus, and extended amygdala to integrate HPA axis activation not only in response to an acute stressor but also in stressor response that is conditioned by past experience? Glucocorticoids play an important role in this plasticity, both acutely and long term, and at virtually all levels: hippocampus, extended amygdala, hypothalamus, and pituitary (Radley et al., 2011). A second, corollary question is to what extent do inputs from the periphery besides glucocorticoids, such as peripheral catecholamine release from sympathetic nerves and the adrenal medulla, also promote plasticity in brain stress response circuitry? The chapters following represent major steps forward in framing these questions, a new and expanded understanding of the neurochemistry and neuroanatomy of catecholamine–neuropeptide interactions during the stress response.

CNScentral nervous system
CRHcorticotropin-releasing hormone
HPA axishypothalamic–pituitary adrenal axis
HSA axishormonal sympathetic adrenal axis
LClocus coeruleus
PACAPpituitary adenylate cyclase-activating polypeptide
PFCprefrontal cortex
PGinucleus paragigantocellularis lateralis
PVHparaventricular hypothalamus
SNSsympathetic nervous system

CONFLICT OF INTEREST The author has no conflicts of interest to declare.

Publisher's Disclaimer: This chapter was originally published in the book Advances in Pharmacology, Vol.

68, published by Elsevier, and the attached copy is provided by Elsevier for the author's benefit and for the benefit of the author's institution, for non-commercial research and educational use including without limitation use in instruction at your institution, sending it to specific colleagues who know you, and providing a copy to your institution's administrator.

  • Itoi K, Ohara S, Kobayashi K. Selective ablation of dopamine beta-hydroxylase neurons in the brain by immunotoxin-mediated neuronal targeting. Advances in Pharmacology. this volume. [PubMed] [Google Scholar]
  • McEwen BS. Central effects of stress hormones in health and disease: Understanding the protective and damaging effects of stress and stress mediators. European Journal of Pharmacology. 2008;583:174–185. [PMC free article] [PubMed] [Google Scholar]
  • Radley JJ, Kabbaj M, Jacobson L, Heydendael W, Yehuda R, Herman JP. Stress risk factors and stress-related pathology: Neuroplasticity, epigenetics and endophenotypes. Stress. 2011;14:481–497. [PMC free article] [PubMed] [Google Scholar]
  • Stroth N, Holighaus Y, Ait-Ali D, Eiden LE. PACAP: A master regulator of neuroendocrine stress circuits and the cellular stress response. Annals of the New York Academy of Sciences. 2011;1220:49–59. [PMC free article] [PubMed] [Google Scholar]

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3928117/

Development of catecholamine and cortisol stress responses in zebrafish

All About Catecholamines in the Stress Response

1. Hashiguchi H., Ye S.H., Morris M., Alexander N. Single and repeated environmental stress: effect on plasma oxytocin, corticosterone, catecholamines, and behavior. Physiol. Behav. 1997;61:731–736. [PubMed] [Google Scholar]

2. Kvetnansky R., Pacak K., Fukuhara K., Viskupic E., Hiremagalur B., Nankova B., Goldstein D.S., Sabban E.L., Kopin I.J. Sympathoadrenal system in stress — interaction with the hypothalamic–pituitary–adrenocortical system. Ann. N. Y. Acad. Sci. 1995;771:131–158. [PubMed] [Google Scholar]

3. Kvetnansky R., Kubovcakova L., Tillinger A., Micutkova L., Krizanova O., Sabban E.L. Gene expression of phenylethanolamine N-methyltransferase in corticotropin-releasing hormone knockout mice during stress exposure. Cell. Mol. Neurobiol. 2006;26:735–754. [PubMed] [Google Scholar]

4. Kvetnansky R., Krizanova O., Tillinger A., Sabban E.L., Thomas S.A., Kubovcakova L. Regulation of gene expression of catecholamine biosynthetic enzymes in dopamine-beta-hydroxylase- and CRH-knockout mice exposed to stress. Ann. N. Y. Acad. Sci. 2008;1148:257–268. [PMC free article] [PubMed] [Google Scholar]

5. Meaney M.J., Diorio J., Francis D., Widdowson J., LaPlante P., Caldji C., Sharma S., Seckl J.R., Plotsky P.M. Early environmental regulation of forebrain glucocorticoid receptor gene expression: implications for adrenocortical responses to stress. Dev. Neurosci. 1996;18:49–72. [PubMed] [Google Scholar]

6. Natelson B.H., Tapp W.N., Adamus J.E., Mittler J.C., Levin B.E. Humoral indices of stress in rats. Physiol. Behav. 1980;26:1049–1054. [PubMed] [Google Scholar]

7. Pacak K., Palkovits M., Kvetnansky R., Yadid G., Kpoin I.J., Goldstein D.S. Effects of various stressors an in vivo norepinephrine release in the hypothalamic paraventricular nucleus and on the pituitary-adrenocortical axis. Ann. N. Y. Acad. Sci. 1995;771:115–130. [PubMed] [Google Scholar]

8. Sabban E.L., Liu X., Serova L., Gueorguiev V., Kvetnansky R. Stress triggered changes in gene expression in adrenal medulla: transcriptional responses to acute and chronic stress. Cell. Mol. Neurobiol. 2006;26:845–856. [PubMed] [Google Scholar]

9. Bornstein S.R., Tian H., Haidan A., Bottner A., Hiroi N., Eisenhofer G., McCann S.M., Chrousos G.P., Roffler Tarlov S. Deletion of tyrosine hydroxylase gene reveals functional interdependence of adrenocortical and chromaffin cell system in vivo. PNAS USA. 2000;97:14742–14747. [PMC free article] [PubMed] [Google Scholar]

10. Alsop D., Vijayan M.M. Development of the corticosteroid stress axis and receptor expression in zebrafish. Am. J. Physiol. 2008;294:R2021–R2024. [PubMed] [Google Scholar]

11. Alsop D., Vijayan M.M. Molecular programming of the corticosteroid stress axis during zebrafish development. Comp. Biochem. Physiol. 2009;153:49–54. [PubMed] [Google Scholar]

12. Alsop D., Vijayan M. The zebrafish stress axis: molecular fallout from the teleost-specific genome duplication event. Gen. Comp. Endocrinol. 2009;161:62–66. [PubMed] [Google Scholar]

13. Powers J.W., Mazilu J.K., Lin S., McCabe E.R. The effects of hypoglycemia on adrenal cortex function and steroidogenesis in zebrafish. Mol. Genet. Metab. 2010;101:421–422. [PubMed] [Google Scholar]

14. Steele S.L., Ekker M., Perry S.F. Interactive effects of development and hypoxia on catecholamine synthesis and cardiac function in zebrafish (Danio rerio) J. Comp. Physiol. 2011;181:527–538. [PubMed] [Google Scholar]

15. Stouthart A., Lucassen E., van Strien F.J., Balm P.H., Lock R.A., Wendelaar Bonga S.E. Stress responsiveness of the pituitary-interrenal axis during early life stages of common carp (Cyprinus carpio) J. Endocrinol. 1998;157:127–137. [PubMed] [Google Scholar]

16. Briggs J.P. The zebrafish: a new model organism for integrative physiology. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2002;282:R3–R9. [PubMed] [Google Scholar]

17. Penberthy W.T., Shafizadeh E., Lin S. The zebrafish as a model for human disease. Front. Biosci. 2002;7:d1439–d1453. [PubMed] [Google Scholar]

18. Westerfield M. 4th ed. Univ. of Oregon Press; Eugene: 2000. The Zebrafish Book. A Guide for the Laboratory Use of Zebrafish (Danino rerio) [Google Scholar]

19. 7th ed. National Research Council, National Academies Press; Washington, D.C.: 1996. Guide for the Care and Use of Laboratory Animals. [Google Scholar]

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5121345/

The Differences between Catecholamines and Cortisol

All About Catecholamines in the Stress Response

Updated April 25, 2017

By Lizzie Brooks

Catecholamines and cortisol are both chemical messengers in the human body, and both are involved in the human stress response, among other functions.

Catecholamines are a group of chemicals that include epinephrine, norepinephrine, and dopamine, all of which function both as neurotransmitters and as hormones in the body.

Cortisol is a single chemical whose main functions include the regulation of metabolism, as well as the regulation of other hormones.

Cortisol is synthesized and released by the human adrenal cortex, the outermost portion of the adrenal glands, located just above each kidney, whereas catecholamines are synthesized in the adrenal medulla of the brain, as well as inside some sympathetic nerve fibers.

Catecholamines contain a benzene ring with adjacent hydroxyl groups and an amine group on the side chain, according to “The Bantam Medical Dictionary.” Cortisol is synthesized from cholesterol and transformed first into progesterone and then into 17-OH-Progesterone, 11-Deoxycortisol, and finally into cortisol by the action of various enzymes.

Receptors for catecholamines are found throughout the body. Epinephrine, also known as adrenaline, can quickly increase heart rate, rate of respiration, and rate of re-absorption of water and signal other subtle changes in the body that facilitate the fight-or-flight response.

The effects of cortisol can be seen only after 30 minutes at the earliest and usually not for hours or days. Norepinephrine, a chemical related to epinephrine, can signal the release of cortisol to prepare the body for long-term stress.

Cortisol inhibits growth and reproductive functions and establishes a metabolism suited to quick action or future famine, such as high blood sugar and the storage of fat.

An excess of cortisol can result in a condition known as Cushing's syndrome. This disease can result from injury or tumors on the adrenal glands or other glands in the body or from taking certain medications, such as prednisone, for a prolonged period of time.

Cushing's syndrome is characterized by a lump of fat between the shoulders, rounded face, and progressive obesity and can lead to high blood pressure, bone loss, and occasionally diabetes.

Excessive levels of catecholamines, or the hyperactivity of catecholamine receptors, is believed to be associated with certain types of psychosis, which can be treated by dopamine receptor inhibitors such as the drug chlorpromazine.

A deficiency of cortisol, caused by damage to or disease of the adrenal glands can lead to Addison's disease, characterized by muscle weakness, fatigue, low blood pressure, low blood sugar, irritability, and depression, among other symptoms. The degradation of receptors for catecholamines, specifically for dopamine, is associated with the muscular tremors and rigidity of Parkinson's disease, which can be partially treated with L-dopa, a drug that is a dopamine precursor.

Source: https://sciencing.com/differences-between-catecholamines-cortisol-7472976.html