Plasma epinephrine and norepinephrine

Caffeine causes a rise in plasma epinephrine and norepinephrine in subjects unused to caffeine beverages. 

This blood pressure and the plasma epinephrine and norepinephrine (2 and 3 above) effect of caffeine disappear after a few days, even if heavy coffee consumption continues. 

Ketamine is the only intravenous anesthetic that possesses analgesic properties and produces cardiovascular stimulation. Heart rate, arterial blood pressure, and cardiac output are usually significantly increased. The peak increases in these variables occur 2-4 minutes after intravenous injection and then slowly decline to normal over the next 10-20 minutes. Ketamine produces its cardiovascular stimulation by excitation of the central sympathetic nervous system and possibly by inhibition of the reuptake of norepinephrine at sympathetic nerve terminals. Increases in plasma epinephrine and norepinephrine levels occur as early as 2 minutes after intravenous ketamine and return to baseline levels 15 minutes later. 

A.Yamatodani and H. Wada, Automated analysis for plasma epinephrine and norepinephrine by hquid chromatography, including a sample cleanup procedure. Clin. Chem., 27, 1983-1987 (1981). 

Granados G. Garay-Sevilla ME, Malacara JM, et al Plasma epinephrine and norepinephrine response to... 

In addition to studying hemodynamic changes caused by liberated histamine, plasma epinephrine and norepinephrine levels have been investigated following injection of morphine. In a study of a patient who experienced an anaphylactoid response following the intravenous injection of morphine 0.3 mg/kg, plasma catecholamines were increased and this was accompanied by decreases in systemic vascular resistance and arterial blood pressure. In another study, intravenous morphine increased cardiac output, histamine, and epinephrine plasma concentrations and decreased arterial blood pressure and systemic vasculature resistance in adult subjects with no history of drug allergy or clinical evidence of cardiovascular, pulmonary, or metabolic disease. 

The vesicular monoamine transporters (VMATs) were identified in a screen for genes that confer resistance to the parkinsonian neurotoxin MPP+ [2]. The resistance apparently results from sequestration of the toxin inside vesicles, away from its primary site of action in mitochondria. In addition to recognizing MPP+, the transporter s mediate the uptake of dopamine, ser otonin, epinephrine, and norepinephrine by neurons and endocrine cells. Structurally, the VMATs show no relationship to plasma membrane monoamine transporters. 

In a third study the time course of the effects of intravenous and intracoronary injections of cysteinyl leukotrienes on metabolic parameters and systemic and coronary hemodynamics was examined in patients with normal coronary arteries [32]. LTD4 (3 nmol, injected into the left coronary artery) induced an early (20 s), transient fall in mean arterial pressure paralleled by rises in heart rate and plasma levels of epinephrine and norepinephrine, all of which had returned to baseline by 10 min. CVR rose at 10 and 15 min and myocardial oxygen extraction at 15 min. Thus, small doses of cysteinyl leukotrienes may induce both an early, transient fall in mean arterial pressure, with secondary sympathoadrenergic activation, and a later increase in small coronary arteriolar resistance. 

Several of the neurotransmitters are small-molecule amines such as dopamine, serotonin, epinephrine, and norepinephrine. These neurotransmitters are synthesized in the cytoplasm of the axon terminal and subsequently transported into and stored within the synaptic vesicles. The amino acids glycine and glutamic acid are normal constituents of proteins and are present in abundance in the axons. These are also stored in synaptic vesicles. Each electrical impulse that arrives at the presynaptic side of a synapse will cause only a small minority of the synaptic vesicles to fuse with the plasma membrane and discharge their contents. The remaining synaptic vesicles remain, waiting for subsequent electrical impulses. At the same time, neurotransmitter synthesis continues, as does their storage in synaptic vesicles. This tends to restore the full complement of amine neurotransmitters at the axon terminal. 

In addition to autonomic ganglia, nicotinic receptors are found in a variety of organs, and their stimulation will produce quite different results in these different tissues. Activation of nicotinic receptors on the plasma membrane of the cells of the adrenal medulla leads to the exo-cytotic release of epinephrine and norepinephrine stimulation of nicotinic receptors at the neuromuscular junction results in the contraction of skeletal muscle (see... 

W. M. Manger, Chemical Quantitation of Epinephrine and Norepinephrine in Plasma. Charles C. Thomas, Springfield, 111., 1959. 

The metabolic effects of epinephrine are important during injury. Epinephrine can activate purine metabolism and may contribute to the increased excretion of nitrogen after injury (G9). Epinephrine and norepinephrine promote chemical thermogenesis after injury and thus will contribute to the increased metabolic expenditure of the injury period (S7). Epinephrine will also cause an acute lowering of the plasma albumin with a rise in the a-globulin fraction probably due to the effect on ACTH secretion. 

Heart rate and systolic and diastolic blood pressures are greater in the upright than in the recumbent individual. The change in posture from lying to standing increases the secretion of catecholamines, aldosterone, angiotensin II, renin, and antidiuretic hormone. Epinephrine and norepinephrine concentrations in plasma may double within 10 minutes, but... 

Ward MM, Metford IN, Parker SD, Chesney MA, Taylor CB, Keegan DL, Barchas JD (1983) Epinephrine and norepinephrine responses in continuously collected human plasma to a series of stressors. Psychosomat Med 45 471 86. 

The catecholamines epinephrine and norepinephrine (adrenaline and noradrenaline) originate in the inner medullar region of the adrenal glands. Stimulation of the adrenal by the sympathetic nervous system leads to secretion of catecholamines into the bloodstream. In addition, adipose tissue is itself directly innervated by the sympathetic nervous system. Various types of metabolic stress trigger the sympathetic nervous system to release its neurotransmitter, norepinephrine, directly into adipose where its effects on the adipocyte are mediated by specific plasma membrane adrenoreceptors. Rapid reflex responses are primarily stimulated by the sympathetic nervous system, whereas more long-term (i.e., on the scale of hours, days, and weeks) and/or basal effects are subject to regulation by catecholamine secretion. 

The hormonal changes that direct the inaeased hepatic glycogenolysis, hepatic gluconeogenesis, and adipose tissue include a decrease in insulin and an increase in glucagon, epinephrine, and norepinephrine. Plasma levels of growth hormone, cortisol, and thyroid-stimulating hormone (TSH) also increase and may make a contribution to... 

An optimization procedure for the separation of epinephrine bitartrate, L-DOPA, 3,4-dihydroxyphenylacetic acid, notepinephrine-HCl and dopamine-HCl (with 3,4-dihydroxybenzylamine-HCl as internal standard), was described by He et al. [1075]. A C,8 column was used in conjunction with an electrochemical detector (-1-0.6 V vs, Ag/AgCl). A window diagram of relative retention times for adjacent eluting solute pairs (i.e., lR2/tRi) resulted in three acceptable solvent composition windows. The optimal solvent conditions were found to be 2.5/97.5 acetonitrile/water (0.23% sodium acetate with 0.02% EDTA and 0.066% sodium heptanesulfonate adjusted to pH 3.9 with monochloroacetic acid). Elution was complete in <30 min and all peaks were well resolved. Detection limits for dog or human plasma samples were reported as 10pg/mL for epinephrine and norepinephrine. 

Jacob, K., Vogt, W., and Knedel, M. Quantitation of Epinephrine and Norepinephrine from Human Plasma by High-Resolution Mass Fragmentography... 

Smythe, Ch. McC., Nickel, J. F. and Bradley, S. E., The effect of epinephrine (USP), /-epinephrine, and /-norepinephrine on glomerular filtration rate, renal plasma flow, and the urinary excretion of sodium, potassium, and water in normal man, J. Clin. Invest. 31, 499 (1952). 

The extensive literature about the Upolytic effect of the catecholamines< > should not be reviewed here. Our experiments show ed that epinephrine and norepinephrine at doses higher than those producing maximal effects in mammals do not elevate plasma FFA in the duck. Continuous infusion of either epinephrine or norepinephrine failed to produce fatty liver in the duck, in contrast with their effect in dogs.< ... 

Vasopressin is a peptide hormone produced by the hypothalamus and secreted by the posterior pituitary in response to stimulation. Normal stimuli for vasopressin release are hyperosmolarity and hypovolemia, with thresholds for secretion of greater than 280 mOsm/kg and greater than 20% plasma volume depletion. A number of other stimuli, such as pain, nausea, epinephrine, and numerous drugs, induce release of vasopressin. Vasopressin release is inhibited by volume expansion, ethanol, and norepinephrine. The physiological effect of vasopressin is to promote free water clearence by altering the permeability of the renal collecting duct to water. In addition, it has a direct vasoconstrictor effect. Consequently, vasopressin results in water retention and volume restoration. In patients with septic shock, vasopressin is appropriately secreted in response to hypovolemia and to elevated serum osmolarity (R14). 

Figure 15 Chromatograms of catecholamines obtained from (a) human and (b) Sprague-Dawley rat plasma. Peaks NE = norepinephrine E = epinephrine I = 3,4-dihydroxybenzylamine DA = dopamine. (From Ref. 88.)...

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