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Epinephrine

Epinephrine (INN), also epinephrin (both pronounced ep-i-NEF-rin), or adrenaline (BAN) is a hormone and a neurotransmitter. The Latin roots ad-+renes and the Greek roots epi-+nephros both literally mean "on/to the kidney" (referring to the adrenal gland, which secretes epinephrine). Epinephrine is sometimes shortened to epi in medical jargon. more...

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Epinephrine is a catecholamine, a sympathomimetic monoamine derived from the amino acids phenylalanine and tyrosine. Its ATC code is C01CA24.

William Bates reported in the New York Medical Journal in May 1886 the discovery of a substance produced by the suprarenal gland. Epinephrine was isolated and identified in 1895 by Napoleon Cybulski, Polish physiologist. The discovery was repeated in 1897 by John Jacob Abel. Jokichi Takamine discovered the same hormone in 1900, without knowing about the previous discovery; but, in later years, counterevidence is shown from the experiment note that Kaminaka leaves that the Takamine team is the discoverer of first adrenaline. It was first artificially synthesized in 1904 by Friedrich Stolz.

Actions in the body

Epinephrine plays a central role in the short-term stress reaction—the physiological response to threatening or exciting conditions (see fight-or-flight response). It is secreted by the adrenal medulla. When released into the bloodstream, epinephrine binds to multiple receptors and has numerous effects throughout the body. It increases heart rate and stroke volume, dilates the pupils, and constricts arterioles in the skin and gut while dilating arterioles in leg muscles. It elevates the blood sugar level by increasing hydrolysis of glycogen to glucose in the liver, and at the same time begins the breakdown of lipids in fat cells. Epinephrine has a suppressive effect on the adaptive immune system.

Epinephrine is used as a drug to promote peripheral vascular resistance via alpha-stimulated vasoconstriction in cardiac arrest and other cardiac disrhythmias resulting in diminished or absent cardiac output, such that blood is shunted to the body's core. This beneficial action comes with a significant negative consequence, increased cardiac irritability, which may lead to additional complications immediately following an otherwise successful resuscitation. Alternatives to this treatment include vasopressin, a powerful antidiuretic which also promotes peripheral vascular resistance leading to blood shunting via vasoconstriction, but without the attendant increase to myocardial irritability.

Because of its suppressive effect on the adaptive immune system, epinephrine is used to treat anaphylaxis and sepsis. Allergy patients undergoing immunotherapy can get an epinephrine rinse before the allergen extract is administered, thus reducing the immune response to the adminsitered allergen. It is also used as a bronchodilator for asthma if specific beta-2-adrenergic agonists are unavailable or ineffective. Adverse reactions to epinephrine include palpitations, tachycardia, anxiety, headache, tremor, hypertension, and acute pulmonary edema.

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Plasma leptin response to an epinephrine infusion - Leptin
From Nutrition Research Newsletter, 3/1/02

Obesity is the result of an imbalance between energy intake and expenditure. The discovery of leptin has been an important breakthrough in understanding of the regulation of energy balance. Although its presence has been reported in other tissues, leptin is predominantly a product of adipose tissue (AT) and, thus, closely correlates with body fatness. However, variations in plasma leptin concentrations can be observed in the absence of body fatness. The hormonal regulation of leptin production by AT has been widely studied in recent years. So far, insulin and glucocorticoids have been identified as important hormonal modulators of leptin secretion by AT. In addition, the importance of the sympathetic nervous system in the decreased leptin levels associated with fasting is supported in numerous studies. The current study examined the impact of epinephrine administration on plasma leptin concentrations. Although epinephrine is recognized to modulate plasma leptin concentration, potential differences in the leptin response to epinephrine infusion between normal weight and overweight subjects have not been investigated.

The researchers measured plasma leptin, insulin, and free fatty acid (FFA) responses after a 60-minute epinephrine infusion followed by a 30-minute recovery period in a group of 11 lean and 15 obese premenopausal women. Leptin, insulin, and FFA levels were measured in plasma before, and at every 30 minutes over the 90-minute period. Adiposity variables, including body fatness and waist circumference, were significantly higher in obese compared with lean women. The high levels of body fat in obese women were also associated with higher fasting plasma leptin concentrations in obese compared with lean women.

In both lean and obese individuals, plasma leptin was significantly reduced by epinephrine. Body fat mass was associated with fasting leptin levels as well as with the decrease in leptinemia produced by epinephrine administration. There was a large range of leptin responses to epinephrine within the study subjects, especially in obese women. However, there was no association between postepinephrine leptin and FFA levels. Results of the study indicate that leptin levels decrease after epinephrine administration in both lean and obese premenopausal women. However, the heterogeneity in the response of leptin to catecholamines suggests potential alterations of the leptin axis that may contribute to generate a positive energy balance and, thus, may favor weight gain in some obese individuals. Additional studies are needed on the hormonal regulation of leptin concentrations in obese subjects to confirm whether the heterogeneity of the epinephrine-induced leptin response in obese subjects can be associated with any impairment of the regulation of energy balance.

C. Couillard, P. Mauriege, D. Prud'homme, A. Nadeau, A. Tremblay, C. Bouchard, and J. Despres. Plasma leptin response to an epinephrine infusion in lean and obese women. Obesity Research 10(1): 6-13 (January 2002). [Address correspondence to: Dr. Jean-Pierre Despres, Quebec Heart Institute, Laval Hospital Research Center, Mallet Pavilion, 2nd Floor, 2725, Chemin Sainte-Foy, Sainte-Foy, Quebec, Canada, G1V 4G5. E-mail: jeanpierre.despres@crchul.ulaval.ca.]

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