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Norepinephrine

Norepinephrine (INN) or noradrenaline (BAN) is a catecholamine and a phenethylamine with chemical formula C8H11NO3. It is released from the adrenal glands as a hormone into the blood, but it is also a neurotransmitter in the nervous system where it is released from noradrenergic neurons during synaptic transmission. As a stress hormone, it affects parts of the human brain where attention and impulsivity are controlled. more...

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Along with epinephrine, this compound effects the fight-or-flight response, activating the sympathetic nervous system to directly increase heart rate, release energy from fat, and increase muscle readiness.

The host of physiological changes activated by a stressful event are unleashed in part by activation of a nucleus in the brain stem called the locus ceruleus. This nucleus is the origin of most norepinephrine pathways in the brain. Neurons using norepinephrine as their neurotransmitter project bilaterally from the locus ceruleus along distinct pathways to the cerebral cortex, limbic system, and the spinal cord, among other projections.

At synapses it acts on both alpha and beta adrenoreceptors.

Antidepressants

Changes in the norepinephrine system are implicated in depression. Serotonin-norepinephrine reuptake inhibitors (SNRIs) treat depression by increasing the amount of serotonin and norepinephrine available to postsynaptic cells in the brain. There is some recent evidence showing that the norepinephrine transporter also normally transports some dopamine as well, implying that SNRIs may also increase dopamine transmission. This is because SNRIs work by preventing the serotonin and norepinephrine transporter from taking their respective neurotransmitters back to their storage vesicles for later use. If the norepinephrine transporter normally recycles some dopamine too, then SNRIs will also enhance dopaminergic transmission. Therefore, the antidepressant effects associated with increasing norepinephrine levels may also be partly or largely due to the concurrent increase in dopamine (particularly in the prefrontal cortex).

Some other antidepressants (for example some tricyclic antidepressants (TCAs)) affect norepinephrine as well, in some cases without affecting other neurotransmitters (at least not directly).

Role in attention

Norepinephrine, along with dopamine, has come to be recognized as playing a large role in attention and focus. In response, Eli Lilly Pharmaceuticals has released Strattera (atomoxetine), a selective norephinephrine reuptake inhibitor, for the treatment of ADHD in adults and children. Strattera is unique in medications specifically indicated for ADHD, as, unlike the psychostimulants (methylphenidate, dextroamphetamine, Adderall (a racemic mixture of amphetamine salts)), it affects norephinephrine, rather than dopamine. As a result, Strattera has a very low abuse potential and can act 24 hours-per-day. (It should be noted that some antidepressants, including SNRIs, have been used off-label for treatment of ADHD.)

Clinical use

Norepinephrine (commonly referred to by the brand name Levophed) is also a powerful medicine used in critically-ill patients as a vasopressor. It is given intravenously and acts on both alpha-1 and beta-1 adrenergic receptors to cause vasoconstriction. Norepinephrine is mainly used to treat patients in septic shock.

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Should a renal dose of norepinephrine stimulate hyperfiltration in head trauma patients?
From CHEST, 6/1/05 by Francois Vincent

To the Editor:

In the August 2004 issue of CHEST, Albanese and colleagues (1) evaluated the effect of norepinephrine (NE) in 26 patients, especially 12 patients with head trauma without infection. The glomerular filtration rate (GFR) was assessed using the formula (urinary creatinine x urinary flow rate)/serum creatinine in the head trauma group, and the Cockroft and Gault formula, published in 1976, (2) in the septic shock group. We were surprised, despite missing data, that mean the GFR was above the normal value in the head trauma patients, approximately 165 mL/min/ 1.73 [m.sup.2]. This remains significant after NE infusion, with a mean value of approximately 150 mL/min/1.73 [m.sup.2]. A similar observation was previously published by Benmalek et al (3) in 1999. Using the same formula to evaluate GFR in 20 young head trauma patients, also treated with NE, they found values of 132 [+ or -] 22 mL/min/1.73 [m.sup.2]. No more explanation was provided. Renal failure is a common complication observation observed after acute brain injury. (4) Indeed, in our knowledge, no other data concerning the increase of GFR in head trauma patients have been published. To confirm this fact, we retrospectively reviewed the charts of brain-dead patients undergoing renal sharing for transplantation. Data were provided by the Etablissement Francais des Greffes when one of our patients was selected to undergo transplantation. During the last 6 months, 58 renal grafts were proposed, obtained in 58 heart-beating donors. In 20 cases, data concerning the donor were insufficient to evaluate GFR before brain death. We also excluded four patients dead after cardiocirculatory arrest and two who died from meningitis. We studied the 32 remaining patients classified as head trauma or stroke (ischemic or hemorrhagic). With one exception, they were treated with NE to obtain a mean arterial pressure > 75 mm Hg. Data were obtained before brain death. The GFR was calculated using the Cockroft and Gault formula, or the recently proposed Modified Diet in Renal Disease formula. (5) We confirmed the existence of hyperfiltration in patients with head trauma (Table 1). No known factors may explain this fact. There was no difference in age, incidence of diabetes mellitus (one in both groups), body mass index, or use of medications as cimetidine or trimethoprime available to diminish the tubular secretion of creatinine. No woman was pregnant. Two questions arise from this. First is the physiologic comprehension: difference in sympathetic tone, neurotransmitters, use of renal functional reserve, difference in nutritional support? Second is the value to study the "renal" effect of NE in patients with such "supranormal" renal function. Other studies are needed to get answers.

Francois Vincent, MD

Noujoud El-Khoury, MD

Guillaume Bonnard, MD

Eric Rondeau, MD, PhD

Tenon University Hospital

Paris, France

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal. org/misc/reprints.shtml).

Correspondence to: Francois Vincent, MD, Department of Renal Intensive Care Unit, Hopital Tenon, 4, Rue De La Chine, 75020 Paris, France; e-mail: frncsvncnt@aol.com

REFERENCES

(1) Albanese J, Leone M, Garnier F, et al. Renal effects of norepinephrine in septic and nonseptic patients. Chest 2004; 126:534-539

(2) Cockroft DW, Gault MH, Prediction of creatinine clearance from serum creatinine. Nephron 1976; 16:31-37

(3) Benmalek F, Behforouz N, Benoist JF, et al. Renal effects of low-dose dopamine during vasopressor therapy for posttraumatic intracranial hypertension. Intensive Care Med 1999; 25:399-405

(4) Davenport A. Renal replacement therapy in the patient with acute brain injury. Am J Kidney Dis 2001; 37:457-466

(5) Levey AS, Bosch JP, Lewis JB, et al. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Ann Intern Med 1999; 130:461-470

COPYRIGHT 2005 American College of Chest Physicians
COPYRIGHT 2005 Gale Group

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