Catecholamines responses

Schmidt. M.E., Matochik, J.A., Goldstein, D.S., et al. Gender differences in brain metabolic and plasma catecholamine responses to alpha2-adrenoceptor blockade. 

Mazzeo, R. S., P.R. Bender, G.A. Brooks, G.E. Butterfield, B.M. Groves, J.R. Sutton, E.E. Wolfel, and J.T. Reeves (1991). Arterial catecholamine responses during exercise with acute and chronic high altitude exposure. Am. J. Physiol. 261 E419-E424. 

The child s estimated blood volume is 80 mL/kg, which is larger than an adult s on a milliliter per kilogram basis. Therefore, small amounts of blood loss can impair perfusion and decrease circulating blood volume. Children have greater cardiac reserves and catecholamine responses compared with adults, allowing them to compensate for fluid losses from hemorrhage, diarrhea, or lack of oral intake. However, shock and cardiopul-... 

Feuerstein, G., Dimicco, J.A., Ramu, A. and Kopin, I.J. (1981). Effect of indomethacin on the blood pressure and plasma catecholamine responses to endotoxemia. ]. Pharm. Pharmacol, 33, 576-579... 

Catecholamine Responses to Various Occupational Activities for Men and Women (Increase From Nonwork Level)... 

Girardi, N.L., Shaywitz, S.E., Shaywitz, B.A., Marchione, K., Fleischman, S.J., Jones, T.W., Tamborlane, W.V., 1995. Blunted catecholamine responses after glucose ingestion in children with attention deficit disorder. Pediatric Research 38, 539-542. 

Lead workers N = 27, 26 males) mean exposure = 6 years Evaluation of (3-2-adrenoreceptor density and catecholamine responses Workplace exposure Plasma norepinephrine and 3-2-adrenoreceptor density highly correlated with PbB and BP, PbB closely associated with BP Chang et al. (1996)... 

Cheung CY. Fetal adrenal medulla catecholamine response to hypoxia—direct and neural components. Am J Physiol 1990 258 R1340-R1346. 

Adams MB, Simonetta G, McMillen IC. The non-neurogenic catecholamine response of the fetal adrenal to hypoxia is dependant on activation of voltage sensitive Ca " -channels. Dev Brain Res 1996 94 182-189. 

Combined Hj /H2 receptor stimulation by histamine is responsible for vasodilation-related symptoms, such as hypotension, flushing, and headache, as well as for tachycardia stimulated indirecdy through vasodilation and catecholamine secretion. 

Two important pathways for catecholamine metaboHsm are 0-methylation by COMT, which is cytoplasmicaHy localized, and oxidative deamination by the mitochondrial localized enzyme MAO. There are large amounts of MAO in tissues such as the fiver and the heart which are responsible for the removal of most of the circulating monoamine, including some taken in from the diet. Tyramine is found in high concentrations in certain foods such as cheese, and in wine. Normally, this tyramine is deaminated in the fiver. However, if MAO is inhibited, the tyramine may then be converted into octopamine [104-14-37] which may indirecdy cause release of NE from nerve terminals to cause hypertensive crisis. Thus MAO, which is relatively nonspecific, plays an important role in the detoxification of pharmacologically active amines ingested from the diet. 

The distinction between a- and P-adrenergic receptors was first proposed by Ahlquist in 1948 based on experiments with various catecholamine derivatives to produce excitatory (a) or inhibitory (P) responses in isolated smooth muscle systems. Initially, a further subdivision into presynaptic a2- and postsynaptic oq-receptors was proposed. However, this anatomical classification of a-adrenergic recqrtor subtypes was later abandoned. 

Signs and symptoms of sympathetic nervous system activity are invariably found in MH. Levels of catecholamines are markedly increased in MH. Whether activation of the sympathetic nervous system is a primary or a secondary response in the syndrome has not been fully elucidated. Gronert reported that stress-induced sympathetic hyperactivity can initiate a malignant hyperthermic episode in susceptible swine without a triggering agent. Stress-induced MH in humans has been inferred because susceptible families have been shown to have an increased incidence of sudden death. Gronert s reasons that activation of the sympathetic... 

The general picture of muscle contraction in the heart resembles that of skeletal muscle. Cardiac muscle, like skeletal muscle, is striated and uses the actin-myosin-tropomyosin-troponin system described above. Unlike skeletal muscle, cardiac muscle exhibits intrinsic rhyth-micity, and individual myocytes communicate with each other because of its syncytial nature. The T tubular system is more developed in cardiac muscle, whereas the sarcoplasmic reticulum is less extensive and consequently the intracellular supply of Ca for contraction is less. Cardiac muscle thus relies on extracellular Ca for contraction if isolated cardiac muscle is deprived of Ca, it ceases to beat within approximately 1 minute, whereas skeletal muscle can continue to contract without an extraceUular source of Ca +. Cyclic AMP plays a more prominent role in cardiac than in skeletal muscle. It modulates intracellular levels of Ca through the activation of protein kinases these enzymes phosphorylate various transport proteins in the sarcolemma and sarcoplasmic reticulum and also in the troponin-tropomyosin regulatory complex, affecting intracellular levels of Ca or responses to it. There is a rough correlation between the phosphorylation of Tpl and the increased contraction of cardiac muscle induced by catecholamines. This may account for the inotropic effects (increased contractility) of P-adrenergic compounds on the heart. Some differences among skeletal, cardiac, and smooth muscle are summarized in... 

If a series of related chemicals, say noradrenaline, adrenaline, methyladrenaline and isoprenaline, are studied on a range of test responses (e.g. blood pressure, heart rate, pupil size, intestinal motility, etc.) and retain exactly the same order of potency in each test system, then it is likely that there is only one type of receptor for all four of these catecholamines. On the other hand, if, as Ahlquist first found in the 1940s, these compounds give a distinct order of potency in some of the tests, but the reverse (or just a different) order in others, then there must be more than one type of receptor for these agonists. 

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