TY - JOUR
T1 - Vasopressin regulation of renal sodium excretion
AU - Stockand, James D.
N1 - Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 2010/11
Y1 - 2010/11
N2 - Vasopressin promotes renal water reabsorption decreasing excretion of free water to dilute plasma and lower serum osmolality. We have good understanding of the causes, mechanisms and consequences of this vasopressin-dependent renal water movement. In comparison, vasopressin actions on renal electrolytes including sodium excretion and its consequences have been less well understood. This is so for investigation and discussions of the renal actions of vasopressin are framed primarily around water metabolism rather than any direct effect on salt handling. The fact that water moves in biological systems, to include the mammalian kidney, only by osmosis passively down its concentration gradient is implicit in such discussion but often not overtly addressed. This can cause confusion. Moreover, although vasopressin action on renal sodium excretion via the V2 receptor is critical to water transport, it is masked easily being situationalfor instance, dependent on hydration state. It is now clear that an increase in sodium reabsorption along the distal nephron (CNT CD) mediated by activation of the epithelial Na+ channel (ENaC) by vasopressin makes an important contribution to maintenance of the axial corticomedullary osmotic gradient necessary for maximal water reabsorption. Thus, we need to modify slightly our understanding of vasopressin and its renal actions to include the idea that while vasopressin decreases free water excretion to dilute plasma, it does this, in part, by promoting sodium reabsorption and consequently decreasing sodium excretion via ENaC activated along the distal nephron.
AB - Vasopressin promotes renal water reabsorption decreasing excretion of free water to dilute plasma and lower serum osmolality. We have good understanding of the causes, mechanisms and consequences of this vasopressin-dependent renal water movement. In comparison, vasopressin actions on renal electrolytes including sodium excretion and its consequences have been less well understood. This is so for investigation and discussions of the renal actions of vasopressin are framed primarily around water metabolism rather than any direct effect on salt handling. The fact that water moves in biological systems, to include the mammalian kidney, only by osmosis passively down its concentration gradient is implicit in such discussion but often not overtly addressed. This can cause confusion. Moreover, although vasopressin action on renal sodium excretion via the V2 receptor is critical to water transport, it is masked easily being situationalfor instance, dependent on hydration state. It is now clear that an increase in sodium reabsorption along the distal nephron (CNT CD) mediated by activation of the epithelial Na+ channel (ENaC) by vasopressin makes an important contribution to maintenance of the axial corticomedullary osmotic gradient necessary for maximal water reabsorption. Thus, we need to modify slightly our understanding of vasopressin and its renal actions to include the idea that while vasopressin decreases free water excretion to dilute plasma, it does this, in part, by promoting sodium reabsorption and consequently decreasing sodium excretion via ENaC activated along the distal nephron.
KW - renal epithelial cell
KW - renal tubular epithelial cells
KW - tubular epithelium
KW - vasopressin
KW - water-electrolyte balance
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U2 - 10.1038/ki.2010.276
DO - 10.1038/ki.2010.276
M3 - Review article
C2 - 20736986
AN - SCOPUS:77958082326
VL - 78
SP - 849
EP - 856
JO - Kidney International
JF - Kidney International
SN - 0085-2538
IS - 9
ER -