Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.796276
Title: Ionic mechanisms involved in the secretion of sweat
Author: Bovell, Douglas L.
Awarding Body: University of Glasgow
Current Institution: University of Glasgow
Date of Award: 1989
Availability of Full Text:
Access from EThOS:
Access from Institution:
Abstract:
Previous EPXMA studies on sweat glands from the horse and the human demonstrated that a fall in the intracellular concentration of K+ occurs in response to thermal stimulation. There is no similar information on the ionic changes that occur in the sweat glands of the cow, the sheep and the goat, during thermal stress. Moreover, the patterns of sweat output exhibited by the cow, sheep and goat differ to those of the horse and the human. As a first objective sweat glands from the cow, sheep and goat were examined by electron probe x-ray microanalysis (EPXMA) to determine whether the different patterns of sweat output exhibited by these animals, could be explained by changes in the glandular intracellular concentrations of sodium, potassium and chlorine. This study demonstrated, that upon thermal stimulation, there was a significant increase in the intracellular concentration of sodium in the secretory cells of the cow, and trends for chlorine to increase and potassium to decrease. In general the changes were qualitatively the same as those reported in the horse and human after thermal stimulation, and suggests that the cow has a similar mechanism of sweat production. No ionic changes were detected in the secretory fundus of the sheep and the goat indicating that sweat output in these animals is a slow continuous process and that the pattern of sweat output is due to the expulsion of preformed sweat by myoepithelial contraction. Furthermore, the results of the EPXMA studies in the horse and the human contrasted with the findings of electrophysiological studies which failed to detect a K+ efflux from sweat glands upon stimulation. A second objective therefore, was to determine by radiotracer methods if a K+ efflux occurs in sweat glands in response to stimulation. Radioisotopic studies demonstrated that a K+ efflux occurs in the isolated human sweat gland in response to agonist-induced stimulation, and that the nature of the K+ loss differs between cholinergic, a and p adrenergic agonists. The K+ efflux in human sweat glands in response to ACh was resolved into two phases; a transient first phase which persisted under Ca2+-free conditions and a second more sustained phase dependent on extracellular Ca2+. The initial phase has been attributed to a release of Ca2+ from bound intracellular stores and the sustained phase to an influx of Ca2+ into the cell. The response to a-adrenergic agents consisted of a single phase which was sensitive to the presence of extracellular Ca2+. In contrast b-adrenergic stimulation caused a slowly increasing rate of K+ efflux, which was independent of increased intracellular Ca2+. The increase in K+ permeability in response to ACh was further investigated using N+-free and Cl-free conditions. The results of the experiments performed under Na+-free conditions demonstrated that the first phase of the ACh-induced K+ efflux was abolished when NMDG+ was used as a Na+ substituent while the second phase persisted. This result suggests that the ACh-induced release of bound intracellular calcium is dependent on the presence of extracellular Na+. However, when Li+ was used as a Na+ replacement both phases of the response persisted. Lithium is known to support proton extrusion to a limited extent, via a Na+-H+ exchanger, and therefore the results of this study are consistent wth a role for the activation of Na+-H+ exchange in normal stimulus-secretion coupling. The experiments involving Na+-free conditions also demonstrated that consistent responses to ACh could not be evoked in bicarbonate-free media and suggest that the human sweat gland has a requirement for the presence of bicarbonate. The results of the Cl-replacement experiments show that in contrast to the simian sweat gland, the ACh-induced efflux of K+ from the isolated human sweat gland is not reduced using Cl-free conditions. Under these conditions ACh evoked a biphasic increase in the rate of K+ efflux. It appears that the presence of extracellular Cl- is not a prerequisite for the ACh-evoked K+ efflux from human sweat glands. The results of the experiments in this thesis would suggest that no single model of the mechanisms involved in sweat production can be applied in detail to the sweat glands of different species.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.796276  DOI: Not available
Share: