V2 receptor (V2R) differs from V1R primarily in the number of sites susceptible to N-linked glycosylation; the V1R has sites at both the amino-terminus and at the extracellular loop, whereas the V2R has a single site at the extracellular amino-terminus.[1]
The well known antidiuretic effect of vasopressin occurs via activation of V2R.[1] 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 V2R with the Gs signaling pathway, which activates cAMP. Interestingly, the V2R continues to activate Gs after being internalized by β-arrestin rather than being desensitized. This internalized Gs signaling by V2R is explained by the receptors ability to form "mega-complexes" consisting of a single V2R, β-arrestin, and heterotrimeric Gs.[3] 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.[1]
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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. [1]
V 2 receptor[edit]
<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. [1]
The well known antidiuretic effect of vasopressin occurs via activation of V 2 R. [1] 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 . [3] 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. [1]
V 3 receptor[edit]
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 Summary
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