Abstract
Aldosterone indirectly regulates water reabsorption in the distal tubule by regulating sodium reabsorption. However, the direct effect of aldosterone on vasopressin-regulated water and urea permeability in the rat inner medullary collecting duct (IMCD) has not been tested. We investigated whether aldosterone regulates osmotic water permeability in isolated perfused rat IMCDs. Adding aldosterone (500 nM) to the bath significantly decreased osmotic water permeability in the presence of vasopressin (50 pM) in both male and female rat IMCDs. Aldosterone significantly decreased aquaporin-2 (AQP2) phosphorylation at S256 but did not change it at S261. Previous studies show that aldosterone can act both genomically and non-genomically. We tested the mechanism by which aldosterone attenuates osmotic water permeability. Blockade of gene transcription with actinomycin D did not reverse aldosterone-attenuated osmotic water permeability. In addition to AQP2, the urea transporter UT-A1 contributes to vasopressin-regulated urine concentrating ability. We tested aldosterone-regulated urea permeability in vasopressin-treated IMCDs. Blockade of gene transcription did not reverse aldosterone-attenuated urea permeability. In conclusion, aldosterone directly regulates water reabsorption through a non-genomic mechanism. Aldosterone-attenuated water reabsorption may be related to decreased trafficking of AQP2 to the plasma membrane. There may be a sex difference apparent in the inhibitory effect of aldosterone on water reabsorption in the inner medullary collecting duct. This study is the first to show a direct effect of aldosterone to inhibit vasopressin-stimulated osmotic water permeability and urea permeability in perfused rat IMCDs.
Highlights
Aldosterone is a steroid hormone that is produced in the adrenal cortex
We investigated whether aldosterone affects vasopressin-stimulated osmotic water permeability in female and male rat inner medullary collecting duct (IMCD)
Aldosterone male or female ratpresence terminalofIMCDs were perfused with vasopressin and perfused with in the vasopressin
Summary
Aldosterone is a steroid hormone that is produced in the adrenal cortex. Its major renal effect is to regulate electrolyte and water homeostasis in the distal tubule, maintaining blood pressure and extracellular fluid homeostasis through the activation of mineralocorticoid receptors (MR) in epithelial cells [1]. The complex of aldosterone and MR translocates into the nucleus and regulates gene transcription of, among others, the epithelial sodium channel (ENaC) and the signaling proteins and kinases that impact channel and transporter activity, such as serum/glucocorticoid kinases (SGKs). This results in increased apical membrane accumulation and activity of ENaC, increasing sodium reabsorption and subsequent water reabsorption (reviewed in [2,3]). Aldosterone can have rapid effects on sodium chloride cotransport (NCC) in distal convoluted tubules [4], bicarbonate reabsorption in proximal tubules [5], natriuresis [6], and several signaling processes in inner medullary collecting ducts (IMCDs) and other nephron
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