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Thesis (M.S.)--University of Wisconsin--Madison, 1984. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 81-86).

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Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 5 uppsatser.

Thesis (Ph.D. in Clinical Science) -- University of Colorado Denver, 2007. / Typescript. Includes bibliographical references (leaves 130-142). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;

Two investigations were conducted to examine the influence of beta-adrenergic blockade on cardiovascular, respiratory, metabolic, and thermoregulatory responses to maximal and submaximal exercise in both highly trained and untrained subjects. In both studies, subjects received randomized and double-blind oral medication with atenolol (100 mg/day), propranolol (160 mg/day), and placebo. In the first study significant reductions in HR max and ‘VO₂ max resulted during the atenolol and propranolol treatments in both the trained and untrained subjects. However, the reductions in ‘VO₂ max were significantly greater in the trained subjects and both groups experienced their greatest reduction during the propranolol treatment. In all subjects, the magnitude of reduction in HR max was significantly greater than the concomitant decrease in ‘VO₂ max. It is concluded that untrained subjects have a greater compensatory reserve than do trained subjects during maximal exercise while under beta-adrenergic blockade. In addition, significant advantages were found with the use of a selective compared to a non-selective beta blocker. Thermoregulation during prolonged exercise in the heat with beta blockade was studied in fourteen subjects. Subjects performed 90-minute cycle ergometer rides at a workload equivalent to 40% of the subjects' unblocked ‘VO₂ max. Rectal temperature was slightly higher during the atenolol trial compared to the placebo but was not different during the propranolol trial compared to the placebo. Skin blood flow was significantly lower during the propranolol trial compared to both the atenolol and placebo trials, but it did not differ significantly between the atenolol and placebo trials. Maintenance of rectal temperatures appeared to be achieved through changes in sweat rate, skin blood flow, and a reduced heat production, i.e., lower ‘VO₂ during the propranolol trial. The decrease in cutaneous blood flow reported during the propranolol trial is likely associated with the associated increase in TPR. This increase in TPR would help to compensate for the lower ‘Q and, hence, help maintain mean arterial pressure. Changes in substrate utilization, i.e., decreased lipolysis, during the beta-blocked trials may also be indicated. Lastly, the inability of two subjects to complete the 90-minute ride, the elevated RPE values, and the additional side effects reported during the propranolol trial would indicate an advantage for the use of a selective blocker.

Macrófagos são capazes de sintetizar melatonina quando ativados por agonistas de TLRs de forma dependente da ativação da via NF-κB. A melatonina produzida pelos macrófagos está relacionada com o favorecimento da fagocitose de partículas ricas em manose. Catecolaminas são capazes de ativar a via NF-κB em células imunocompetentes, e são produzidas por estas células quando ativadas. É conhecido que a descarga noturna de noradrenalina na glândula pineal é responsável pela produção de melatonina na fase de escuro. Hipotetizamos que catecolaminas, ao exemplo da glândula pineal, pudessem induzir a síntese de melatonina em macrófagos. Avaliamos se agonistas adrenérgicos poderiam regular a produção de melatonina nos macrófagos RAW 264.7. Analisamos também o efeito da melatonina em conjunto com agonistas adrenérgicos no modelo experimental de lesão pulmonar aguda. Ambas catecolaminas foram capazes de aumentar a expressão da enzima AA-NAT total ou fosforilada e induzir a síntese de melatonina, via ativação de β-adrenoceptores; sendo dependente de NF-κB, e não da sinalização mediada por AMPc. A instilação de LPS nos pulmões dos camundongos induz a expressão de Tnf e de Aa-nat, o que é inibido pelo agonista β2-adrenérgico. A melatonina exerce um efeito anti-inflamatório na produção de citocinas in vivo e in vitro, além de inibir a expressão de Nos2 em macrófagos MH-S, sem alterar arginase-1. Os dados aqui apresentados sugerem que a via de sinalização NF-κB faz a integração da sinalização adrenérgica com a produção de melatonina em macrófagos / TLRs-activated macrophages can synthesize melatonin in a NF-κB pathway-mediated manner. Macrophage-produced melatonin is related to the favoring of mannose-rich particles phagocytosis. Catecholamines can trigger NF-κB pathway in immunocompetent cells, and are produced after activation. It is well known that the nocturnal surge of noradrenaline in the pineal gland is responsible for the dark phase melatonin synthesis. We hypothesized that catecholamines, like in pineal gland, could induce melatonin synthesis by macrophages. We evaluated if adrenergic agonists could regulate melatonin production in RAW 264.7 macrophages. We also analyzed the effect of melatonin together with adrenergic agonist in the experimental model of acute lung injury. Both catecholamines were able to increase the expression of total or phosphorylated AA-NAT enzyme, and induce melatonin synthesis through β-adrenoceptor activation; in a NF-κB-dependent way, but not by the cAMP signaling. LPS instillation in the mice lungs induces Tnf and Aa-nat expression, which is inhibited by the β2-adrenergic agonist. Melatonin exerts an anti-inflammatory effect in cytokine production both in vivo and in vitro, besides the inhibition of Nos2 in MH-S macrophages, without changing arginase-1. The presented data suggests that the NF-κB signaling pathway fulfill the integration of adrenergic signaling with melatonin synthesis in macrophages

Pui Lan Wong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1993. / Includes bibliographical references (Leaves 109-122). / Abstract --- p.i / Acknowledgements --- p.iii / Chapter Chapter1 --- Introduction / Chapter 1.1 --- A general introduction on mast cells --- p.1 / Chapter 1.2 --- Activation of mast cells --- p.6 / Chapter 1.3 --- Mediators of mast cells --- p.18 / Chapter 1.4 --- Usage of β-adrenoceptor agonists in asthma therapy --- p.26 / Chapter 1.5 --- Aim of this study --- p.32 / Chapter Chapter2 --- Materials and methods / Chapter 2.1 --- Chemicals --- p.42 / Chapter 2.2 --- Buffers and stock solutions --- p.43 / Chapter 2.3 --- Source of mast cells --- p.45 / Chapter 2.4 --- Animal sensitization --- p.45 / Chapter 2.5 --- Isolation of mast cells --- p.46 / Chapter 2.6 --- Procedure for the investigation of the effects of adrenoceptor agonists on histamine release from mast cells --- p.48 / Chapter 2.7 --- Procedure for the investigation of propranolol antagonism --- p.49 / Chapter 2.8 --- Histamine assay --- p.50 / Chapter 2.9 --- Data analysis --- p.50 / Chapter Chapter3 --- Results / Chapter 3.1 --- Establishment of experimental conditions --- p.53 / Chapter 3.2 --- The effects of β-agonists on immunologically induced histamine release from guinea pig lung mast cells --- p.54 / Chapter 3.3 --- The effects of β-agonists and two anti-allergic drugs on immunologically induced histamine release from guinea pig lung mast cells --- p.56 / Chapter 3.4 --- The effects of β2-agonists on histamine release induced by non-immunological agents from guinea pig lung mast cells --- p.56 / Chapter 3.5 --- Antagonism by propranolol on the effects of β2-agonists on histamine release from guinea pig lung mast cells --- p.57 / Chapter 3.6 --- The effects of β2-agonists on immunologically induced histamine release from rat peritoneal mast cells --- p.58 / Chapter 3.7 --- The effects of β2-agonists on immunologically induced histamine release from human lung mast cells --- p.58 / Chapter 3.8 --- "Comparison of the effects of β2-agonists on immunologically induced histamine release from mast cells isolated from the rat peritoneum, the guinea pig lung and the human lung" --- p.59 / Chapter Chapter4 --- Discussion / Chapter 4.1 --- The effects of β-agonists on immunologically induced histamine release from guinea pig lung mast cells --- p.89 / Chapter 4.2 --- The effects of β2-agonists and two anti-allergic drugs on immunologically induced histamine release from guinea pig lung mast cells --- p.97 / Chapter 4.3 --- The effects of novel β2-agonists on histamine release induced by non-immunological agents from guinea pig lung mast cells --- p.99 / Chapter 4.4 --- The study of propranolol --- p.100 / Chapter 4.5 --- The heterogeneity of mast cells --- p.103 / Chapter Chapter5 --- General conclusion --- p.107 / References --- p.109

Kai Hong Kwok. / Thesis submitted in: December 1997. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 90-98). / Abstract also in Chinese. / Chapter Chapter 1 --- Introduction / Chapter 1.1. --- Classification of β-adrenoceptor in cardiovascular system --- p.1 / Chapter 1.2. --- Vasodilator effects of β-adrenoceptor-agonists and their mechanisms --- p.4 / Chapter 1.3. --- Role of endothelium in β-adrenoceptor-mediated vasodilation --- p.7 / Chapter 1.4. --- Role of K+ channels in β-adrenoceptor-mediated relaxation --- p.11 / Chapter 1.5. --- Other aspect regarding the vascular response to stimulation of B-adrenoceptor --- p.15 / Chapter 1.6. --- Clinical aspect of B-adrenoceptor agents --- p.15 / Chapter Chapter 2 --- Methods and Materials / Chapter 2.1. --- Tissue Preparation --- p.19 / Chapter 2.1.1. --- Preparation of the isolated rat mesenteric artery --- p.19 / Chapter 2.1.2. --- Removal of the functional endothelium --- p.19 / Chapter 2.1.3. --- Organ bath set-up --- p.20 / Chapter 2.1.4. --- Length-tension relationship and an optimal resting tension --- p.22 / Chapter 2.2. --- Experimental Procedure --- p.22 / Chapter 2.2.1. --- Relaxant effects of the B-adrenoceptor agonists --- p.24 / Chapter 2.2.2. --- Effects of putative K+ channel blockers --- p.24 / Chapter 2.2.3. --- Effects of inhibitors of nitric oxide activity --- p.25 / Chapter 2.2.4. --- Effect of indomethacin --- p.25 / Chapter 2.2.5. --- "Effects of K+ channel opener, nitric oxide donor and forskolin" --- p.26 / Chapter 2.3. --- Chemicals and Solutions --- p.26 / Chapter 2.3.1. --- Chemicals and drugs --- p.26 / Chapter 2.3.2. --- Preparation of drug stock solutions --- p.26 / Chapter 2.3.3. --- Solutions --- p.28 / Chapter 2.4. --- Statistical Analysis --- p.28 / Chapter Chapter 3 --- Results / Chapter 3.1. --- Relaxant Effect of Isoprenaline --- p.29 / Chapter 3.1.1. --- Relaxant effect of isoprenaline --- p.29 / Chapter 3.1.2. --- Effects of inhibitors of nitric oxide activity --- p.29 / Chapter 3.1.3. --- Effect of charybdotoxin on the vasorelaxant response to isoprenaline --- p.32 / Chapter 3.1.4. --- Effect of glibenclamide on the vasorelaxant response to isoprenaline --- p.32 / Chapter 3.1.5. --- Effect of TPA+ on isoprenaline-induced relaxation --- p.36 / Chapter 3.1.6. --- Effect of TPA+ in the presence of iberiotoxin or glibenclamide --- p.36 / Chapter 3.1.7. --- Effect of Ba2+ on the vasorelaxant effect of isoprenaline --- p.41 / Chapter 3.1.8. --- Effect of raising extracellular K+ on isoprenaline-mediated relaxation --- p.41 / Chapter 3.2. --- Relaxant Effect of Dobutamine --- p.44 / Chapter 3.2.1. --- Effects of inhibitors of endothelium-derived factors on the relaxant effect of dobutamine --- p.44 / Chapter 3.2.2. --- Antagonism of the effect of dobutamine by β1-adrenoceptor antagonist --- p.44 / Chapter 3.2.3. --- Effects of putative Kca channel blockers on the relaxant effect of dobutamine --- p.51 / Chapter 3.2.4. --- Effect of TPA+ on the relaxant effect of dobutamine --- p.55 / Chapter 3.2.5. --- Effect of raising extracellular K+ on the relaxant effect of dobutamine --- p.55 / Chapter 3.3. --- Relaxant Effect of Fenoterol --- p.57 / Chapter 3.3.1. --- Effect of inhibitors of nitric oxide activity on the relaxant effect of fenoterol --- p.57 / Chapter 3.3.2. --- Effect of charybdotoxin on the relaxant effect of fenoterol --- p.57 / Chapter 3.3.3. --- Effect of TPA+ on the relaxant effect of fenoterol --- p.64 / Chapter 3.3.4. --- Effect of glibenclamide on the relaxant effect of fenoterol --- p.64 / Chapter 3.3.5. --- Effect of raising extracellular K+ on fenoterol-mediated relaxation --- p.64 / Chapter 3.4. --- Effects of cAMP- and cGMP-elevating agents --- p.69 / Chapter 3.4.1. --- Effects of inhibitors of endothelium-derived factors on the relaxation induced by nitroprusside and forskolin --- p.69 / Chapter 3.4.2 --- Effect of charybdotoxin on relaxant effect of forskolin --- p.69 / Chapter 3.4.3 --- Effect of Ba2+ on the vasorelaxant effect of forskolin --- p.76 / Chapter 3.4.4 --- Effect of TPA+ on the relaxant effect of forskolin --- p.76 / Chapter 3.4.5 --- Effect of glibenclamide on the relaxant effects of forskolin and cromakalim --- p.76 / Chapter Chapter 4 --- Discussion / Chapter 4.1. --- Effect of Isoprenaline and Fenoterol --- p.77 / Chapter 4.2. --- Effect of Dobutamine --- p.83 / Chapter 4.3. --- Conclusion --- p.88 / References --- p.90 / Publications --- p.98