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Open it plexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s .  The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct <span>principal cells, increasing water reabsorption. <span><body><html>
Original toplevel document
Vasopressin receptor - Wikipedia luminal membrane of the collecting duct limit the antidiuretic action of vasopressin. Additionally, vasopressin selectively contracts efferent arterioles probably through the V 1 R, but not the afferent arteriole. 
V 2 receptor
<span>V 2 receptor (V 2 R) differs from V 1 R primarily in the number of sites susceptible to N-linked glycosylation; the V 1 R has sites at both the amino-terminus and at the extracellular loop, whereas the V 2 R has a single site at the extracellular amino-terminus. 
The well known antidiuretic effect of vasopressin occurs via activation of V 2 R.  Vasopressin regulates water excretion from the kidney by increasing the osmotic water permeability of the renal collecting duct – an effect that is explained by coupling of the V 2 R with the G s signaling pathway, which activates cAMP. Interestingly, the V 2 R continues to activate G s after being internalized by β-arrestin rather than being desensitized. This internalized G s signaling by V 2 R is explained by the receptors ability to form "mega-complexes" consisting of a single V 2 R, β-arrestin, and heterotrimeric G s .  The increased intracellular cAMP in the kidney in turn triggers fusion of aquaporin-2-bearing vesicles with the apical plasma membrane of the collecting duct principal cells, increasing water reabsorption. 
V 3 receptor
The human V 3 receptor (V 3 R, previously known as V 1B R) is a G-protein-coupled pituitary receptor that, because of its scarcity, was only recently characteri
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