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Open AccessDissertation10.25959/23233922

Vascular involvement in skeletal muscle metabolism

Tristram P. D. Eldershaw-1996-01-01-UTAS Research Repository

TL;DRAbstract

Perfused hindlimb preparations have been used to investigate vasoconstrictormediated control of skeletal muscle metabolism, with particular emphasis on the regulation of oxygen consumption (V0 2) as an index of muscle nonshivering thermogenesis (NST). The ability of a group of molecules known as vanilloids to modulate muscle V02 was investigated using hindlimb preparations of hooded Wistar rats. Both naturally-occurring and synthetic vanilloids were examined. Infused vanilloids gave dose-dependent V02 changes in association with increased perfusion pressure (PP). Vanilloid V02 concentration-response curves were biphasic, lower concentrations stimulating and higher concentrations inhibiting V02. Nitrovasodilators demonstrated an association between the V02 changes and vasoconstriction, whilst a- and 13-adrenergic antagonists showed that neither adrenergic receptors nor secondary catecholamine release were responsible for the increased V02. The observed effects may have been due to speci

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Perfused hindlimb preparations have been used to investigate vasoconstrictormediated control of skeletal muscle metabolism, with particular emphasis on the regulation of oxygen consumption (V0 2) as an index of muscle nonshivering thermogenesis (NST). The ability of a group of molecules known as vanilloids to modulate muscle V02 was investigated using hindlimb preparations of hooded Wistar rats. Both naturally-occurring and synthetic vanilloids were examined. Infused vanilloids gave dose-dependent V02 changes in association with increased perfusion pressure (PP). Vanilloid V02 concentration-response curves were biphasic, lower concentrations stimulating and higher concentrations inhibiting V02. Nitrovasodilators demonstrated an association between the V02 changes and vasoconstriction, whilst a- and 13-adrenergic antagonists showed that neither adrenergic receptors nor secondary catecholamine release were responsible for the increased V02. The observed effects may have been due to speci

Keywords

ChemistryVasoconstrictionReceptorInternal medicineVascular smooth muscleThermogenesisEndocrinologySkeletal muscle

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