It is the onlyaquaporin regulated byvasopressin.[5]The basic job of aquaporin 2 is to reabsorb water from the primary urine that flows into the nephron from the filtration of blood in the glomerulus through the Bowman's capsule.[6] Aquaporin 2 is in kidney epithelial cells and usually lies dormant in intracellular vesicle membranes. When it is needed, vasopressin binds to the cell surface vasopressin receptor thereby activating a signaling pathway that causes the aquaporin 2 containing vesicles to fuse with the plasma membrane, so the aquaporin 2 can be used by the cell.[7]This aquaporin is regulated in two ways by thepeptide hormonevasopressin:
short-term regulation (minutes) through trafficking of AQP2 vesicles to the apical region where they fuse with the apical plasma membrane
long-term regulation (days) through an increase inAQP2 gene expression.
This aquaporin is also regulated by food intake. Fasting reduces expression of this aquaporin independently of vasopressin.
Mutations in this channel are associated withnephrogenic diabetes insipidus, which can be autosomal dominant or recessive. Mutations in the vasopressin receptor cause a similar X-linked phenotype.
Lithium, which is often used to treatbipolar disorder, can cause acquireddiabetes insipidus (characterized by the excretion of large volumes of dilute urine) by decreasing the expression of theAQP2 gene.
The expression of theAQP2 gene is increased during conditions associated with water retention such aspregnancy andcongestive heart failure.
^"Human PubMed Reference:".National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:".National Center for Biotechnology Information, U.S. National Library of Medicine.
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^Koeppen BM, Stanton BA (2019).Renal Physiology, Sixth Edition (6th ed.). Philadelphia, PA: Elsevier. pp. 25–40.ISBN9780323595681.
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