Linked Life Data

11370243

Source:http://linkedlifedata.com/resource/pubmed/id/11370243

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pubmed-article:11370243pubmed:abstractTextThe effect of 'chemical sympathectomy', produced by daily intraperitoneal injections of guanethidine sulphate for six weeks, was studied in sedentary rats and in rats chronically exercised by swimming. The guanethidine-treatment itself caused the following changes. There was a reduction in the rate of weight gain resulting in a 7% lower final body weight. Organ content of noradrenaline was decreased by 90% in spleen and submandibular glands and by 83% in the heart. Urinary excretion of noradrenaline was also decreased, but to a lesser degree, both during rest (45% lower) and after acute exercise (46% lower), while the urinary excretion of adrenaline was no different from that of controls. There was a compensatory adrenal hypertrophy in the guanethidine-treated rats, with a significant increase in adrenal catecholamine levels that was more pronounced for noradrenaline (+45%) than for adrenaline (+11%). Chronic physical exercise produced the expected degree of cardiac hypertrophy in untreated rats, but this adaptive cardiac hypertrophy was completely absent in the exercised guanethidine-treated rats. The results indicate, firstly that a good degree of chemical sympathectomy was obtained and that the persistence of a considerable urinary excretion of catecholamines in the guanethidine-treated rats was due to a compensatory increase in the secretory activity of the adrenal medulla. Secondly, it is suggested that the adaptive cardiac hypertrophy produced by chronic exercise is not caused by a direct effect of the increased work load on the cardiac muscle cell, but is instead mediated by release of a trophic factor from cardiac sympathetic nerves, probably noradrenaline itself but possibly a secretory protein.lld:pubmed
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pubmed-article:11370243pubmed:articleTitlePrevention of exercise-induced cardiac hypertrophy in rats by chemical sympathectomy (guanethidine treatment).lld:pubmed
pubmed-article:11370243pubmed:affiliationDepartment of Physiology I, Karolinska Institute, S-104 01 Stockholm, Sweden.lld:pubmed
pubmed-article:11370243pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11370243pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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