Abstract
This article will detail models of aldosterone action in target epithelia such as kidney and toad bladder with respect to Na transport. The renal target cell responsible for aldosterone-dependent Na reabsorption is considered to be the cortical collecting tubule (CCT), while that responsible for acid secretion is characterized by the inner strip of the outer medullary collecting duct.1 An analogous situation is found in toad bladder, with one cell type (granular cell) responsible for aldosterone-dependent Na reabsorption while another (mitochondrial-rich cell) modulating acid secretion in response to steroid.2 With respect to K transport, these two tissues differ, in that aldosterone does not modify the secretory rate of K in the toad bladder due to a vanishingly small apical membrane K permeability, while in the mammalian kidney, aldosterone both increases the urinary excretion of K and the secretion of K by CCTs under steady-state conditions.3–5 With regard to the Na reabsorbing cell, the following paragraphs will both detail existing data and the various working hypotheses currently being evaluated to interpret that data with respect to the means by which aldosterone alters (a) luminal membrane Na permeability, and (b) NaK ATPase activity. In addition, the possible roles of energy and phospholipid metabolism in this process will be discussed. Since some actions of aldosterone parallel those of ADH (antidiuretic hormone), data on both hormones will be contrasted as appropriate in order to help narrow the possible explanations into a cohesive model for the Na reabsorbing cell.
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Marver, D. (1986). Models of Aldosterone Action on Sodium Transport: Emerging Concepts. In: Chrousos, G.P., Loriaux, D.L., Lipsett, M.B. (eds) Steroid Hormone Resistance. Advances in Experimental Medicine and Biology, vol 196. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5101-6_11
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DOI: https://doi.org/10.1007/978-1-4684-5101-6_11
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