Investigation of the primary stimulus and mechanism of the ammonium chloride-induced increase in the content of potassium in choroid plexus epithelial cells

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Title Investigation of the primary stimulus and mechanism of the ammonium chloride-induced increase in the content of potassium in choroid plexus epithelial cells
Publication Type dissertation
School or College College of Pharmacy
Department Pharmacology & Toxicology
Author Harbut, Ronald Eugene Daniel
Date 1983-06
Description After young adult male rate were injected intraperitoneally with NH4C1, the content of K (hereafter, CP [K]) within the epithelial cells of the choroid plexus increased greatly while that of Na (CP [K]) decreased. This dissertation has focused on elucidating the primary stimulus and mechanism of the NH4C1-induced increase in CP [K], with some investigative focus on the induced decrease in CP [Na]. The primary stimuli under consideration are the NH4C1-induced increases in plasma [NH4], [K]. and [H], and decreases in [HCO3] and [Na]. An acidosis-induced augmentation in the concentration of catecholamines available to CP beta-adrenoceptors has also been considered. Since sympathectomy, adrenalectomy or pretreatment with beta-adrenoceptor blockers did not reduce the effects of NH4C1, it was possible to rule out an involvement of catecholamines as the stimulus. A comparison of the time-courses of plasma [ammonia] with CP [K] and [Na} indicated that the primary stimulus was not plasma [NH4]. A comparison of the effects of nine individual salt treatments on plasma [K] with CP [K] and [Na}, revealed that plasma [K] was not the primary stimulus. Significant statistical correlations were drawn between plasma [H] and the induce increase in CP [K] and decrease in CP [Na]. Since an elevation of plasma [H] was most consistently associated with and increase in CP [K], the mechanism through which [H] operates was investigated. The increase in CP [K] and decrease in CP [Na] must result from wither an increase in Na-k exchange (Na-K Atpase), or from a decrease in K efflux and Na influx; or perhaps a combination of both. With a physiological analog of K (i.e., Rb), it was demonstrated that acidosis does not increase the slope of the initial ‘linear uptake of 86Rb in vitro; thus no effect of acidosis to increase Na-Rb exchange (i.e., Na-K exchange) was found. Since acidosis augments the steady-state volume of distribution of 86Rb in vitro, without an increase in Na-Rb exchange, it would appear that acidosis augments CP Rb by effecting a reduction in Rb efflux and, by analogy, would also reduce the efflux of CP K. In conclusion, NH4C1 induces an increase in CP [K] by increasing plasma [H] which in turn acts to reduce the efflux of K across the apical and/or basolateral membranes of the CP. An in vivo indication that acidosis reduces the efflux of K across the apical membrane was suggested by a decrease in CSF [K].
Type Text
Publisher University of Utah
Subject Metabolism; Potassium
Subject MESH Choroid Plexus; Ammonium Chloride; Biological Transport
Dissertation Institution University of Utah
Dissertation Name PhD
Language eng
Relation is Version of Digital reproduction of "Investigation of the primary stimulus and mechanism of the ammonium chloride-induced increase in the content of potassium in choroid plexus epithelial cells." Spencer S. Eccles Health Sciences Library. Print version of "Investigation of the primary stimulus and mechanism of the ammonium chloride-induced increase in the content of potassium in choroid plexus epithelial cells." available at J. Willard Marriott Library Special Collection. QP 6.5 1983 H37.
Rights Management © Ronald Eugene Daniel Harbut.
Format application/pdf
Format Medium application/pdf
Format Extent 3,420,262 bytes
Identifier undthes,5224
Source Original: University of Utah Spencer S. Eccles Health Sciences Library (no longer available).
Funding/Fellowship United States Public Health Service Grants Gm 07579 and NS 13988.
Master File Extent 3,420,318 bytes
ARK ark:/87278/s68054h8
Setname ir_etd
ID 191913
Reference URL https://collections.lib.utah.edu/ark:/87278/s68054h8
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