Adrenergic compounds

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... 

The ability of pyruvate decarboxylase from many microbial sources to produce phenylacetylcarbinol has been exploited for many years in the synthesis of ephedrine, a natural adrenergic compound (92). The acyloin is reductively aminated to produce the ethanolamine product, (1R,2S)-ephediine, with two chiral centers. 

Chiarino et al. [43] described some potent and remarkably selective (3o-adrenoceptor agonists in a series of l-(3-substituted-5-isoxazolyi)-2-alkyl-aminoethanol derivatives in which the isoxazole ring replaces the catechol moiety in the (3-adrenergic compounds. From this series, the compound broxaterol (1) displayed a marked selectivity toward (32-receptors of the trachea and was selected for further development as a potential bronchodilatory agent. 

Structure-Activity Relationship of Adrenergic Compounds That Act on Adenyl Cyclase of the Frog Erythrocyte Ora M. Rosen 6, 227... 

The adrenergic compounds oxjrmetazoline and xylometazoline are potent non-selective 5-HTib ligands (Table 7). 

Chap. 22 Adrenergic Compounds and Adenyl Cyclase Rosen 229... 

Denavit-Sauhie M, Champagnat J, Rondouin G. Central effect of adrenergic compounds on cat respiratory mechanisms. In Fuxe K, Goldstein B, Hdckfelt B, Hockfelt T, eds. Central Adrenaline Neurons Basic Aspects and Their Role in Cardiovascular Functions. Oxford Pergamon, 1980 277-287. 

Jenne JW, Ahrens RC. Pharmacokinetics of heta-adrenergic compounds. In Jenne JW, Murphy S, eds. Drag Therapy for Asthma. New York Marcel Dekker, 1987 213. 

Somatotropin, the P-adrenergic agonists, and the anaboHc steroids are considered metaboHsm modifiers because these compounds alter protein, Hpid, carbohydrate, mineral metaboHsm, or combinations of these and they partition nutrient use toward greater rates of protein deposition, ie, muscle growth, and lesser rates of Hpid accretion. Historical data leading to understanding of the mechanism (s) of action are found in reviews on anaboHc steroids (1), somatotropin (2—4), and the phenethano1 amines (5—7). 

Unlike aniracetam, pramiracetam does not appear to interact with dopaminergic, serotonergic, or adrenergic neurotransmission (72). The agent inhibits prolylendopeptidase in certain brain areas, but its inhibition constant, iC, is only 11 ]lM (69). The absence or weak activity of this compound with various neuronal systems appears to make it less likely to be of significant therapeutic value than other members of this class of agents. 

Selected for clinical trials as a compound to calm agitated patients, imipramine was relatively ineffective. However, it was observed to be effective in the treatment of certain depressed patients (38). Early studies on the mechanism of action showed that imipramine potentiates the effects of the catecholamines, primarily norepinephrine. This finding, along with other evidence, led to the hypothesis that the compound exerts its antidepressant effects by elevating norepinephrine levels at central adrenergic synapses. Subsequent studies have shown that the compound is a potent inhibitor of norepinephrine reuptake and, to a lesser extent, the uptake of serotonin, thus fitting the hypothesis that had been developed to explain the antidepressant actions ofMAOIs. 

A special feature of the iris is its autonomic innervation. Sympathetic activation widens the aperture of the iris whereas impulses from the parasympa thetic nervous system decrease the aperture size. Therefore adrenergic agonists and anticholinergic compounds both increase the aperture of the iris, i.e., cause mydriasis, and antiadrenergic and cholinergic agonists decrease it, i.e., cause miosis. The iris can thus be considered an excellent mirror reflecting the balance of the autonomic nervous system in the body. " ... 

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