Abstract
Arginine vasopressin (AVP), also known as vasopressin or anti-diuretic hormone, is a neuropeptide produced in the hypothalamus. It is primarily responsible for osmoregulation and thus maintains body fluid homeostasis. It is also a potent vasoconstrictor, may have a role in higher cognitive functions and affects metabolism. All the biological and cellular effects of vasopressin are mediated by the interaction of this hormone with three G-protein-coupled receptors – V1a, V1b and V2.Urological applications are based on the rationale that V2 receptors mediate water conservation and increase urine osmolality. Due to their anti-diuretic properties mediated by the V2 receptors, synthetic vasopressin agonists, such as desmopressin, are now commonly used for the treatment of nocturnal polyuria, central diabetes insipidus and nocturnal enuresis and potentially in urinary incontinence. Desmopressin has been licenced worldwide for haematological indications of haemophilia and von Willebrand disease. Vasopressin receptor antagonists correct hyponatremia by blocking the activation of the V2 receptor and induce a free water diuresis without an accompanying natriuresis or kaliuresis; an effect termed ‘aquaresis’. Interfering with vasopressin signalling by administering vasopressin antagonists may have clinical benefits in acute and chronic heart failure.
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Pisipati, S., Hashim, H. (2011). Vasopressin Receptors in Voiding Dysfunction. In: Andersson, KE., Michel, M. (eds) Urinary Tract. Handbook of Experimental Pharmacology, vol 2011. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-16499-6_21
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