Vasopressin Receptor

The actions of vasopressin are mediated by stimulation of tissue-specific G protein-coupled receptors (GPCRs) called vasopressin receptors that are classified into V1, V2 and V3 subtypes. These three subtypes differ in localization, function and signal transduction mechanisms.

113-79-1
Argipressine
113-79-1
1245620-47-6
Ribuvaptan
1245620-47-6
OPC 21268
131631-89-5
138470-70-9
138470-70-9
150683-30-0
Tolvaptan
150683-30-0
TASP 0390325
1642187-96-9
B0084-060541
Desmopressin
16679-58-6
B0084-060639
VPA-985
168079-32-1
168626-94-6
Conivaptan HCl
168626-94-6
210101-16-9
Conivaptan
210101-16-9
347887-36-9
Fedovapagon
347887-36-9
d[leu4,Lys8]-VP
42061-33-6
SSR 149415
439687-69-1
TC OT 39
479232-57-0
d[Cha4]-AVP
500170-27-4

Background


An overview of vasopressin receptor

Vasopressin (AVP) in the body is mainly responsible for regulating water absorption, maintenance of body fluid osmotic pressure, blood volume, blood pressure, cell contraction and proliferation, secretion of adrenocortical hormone and other aspects, and these physiological functions are produced by binding to its receptors. The AVP receptor belongs to the G protein coupled receptor.

Major types of vasopressin receptor

The AVP receptor has 3 subtypes, including V1a receptor (V1aR), V1b receptor (V1bR) and V2 receptor (V2R), and their distribution in vivo and signaling mechanisms are different. V1aR is located in the vascular smooth muscle to mediate the vessel contraction and stimulate the prostate formation. V1bR is located in the anterior pituitary and mediates the release of adrenocorticotrophic hormone (ACTH). And the V2R is located in the basal side membrane of the renal manifold cells.

Inhibition of vasopressin receptor

Conivaptan is a combined V1aR/V2R antagonist, theoretically mitigating the V1aR-induced effects of selective V2R antagonists, especially in patients with CHF. Conivaptan can increase the blood sodium. Obviously, the effect is dose dependent, and the high dosage group has a faster effect.

Vasopressin receptor and diseases

Cushing's syndrome is caused by the chronic overproduction of glucocorticosteroids in the adrenal cortex due to a variety of causes, also known as hypercortisolism. The first-line treatment for Cushing's syndrome is to surgically remove a tumor that secretes excessive ACTH or cortisol, but not all patients have a good surgical outcome. Therefore, it is very important to develop new and effective drugs for the treatment of Cushing's syndrome. In normal pituitary, V3 receptors are expressed in ACTH cells, and vasopressin acts on the V3 receptor. Although its own function of stimulating ACTH secretion is weak, it can significantly enhance the role of CRH to promote ACTH release. The common cause of endocrine tumor formation or high function expression is the activation of intracellular signaling pathway, especially the pathway regulated by G-protein-coupled receptor. Studies have found that ACTH secretion is regulated by cAMP and PLC signaling pathways, and CRH receptors and V receptors play an important role in activating these two signaling pathways. The CRH receptor mainly regulates the secretion of ACTH through the cAMP pathway, and the V receptor is mainly regulated by the PLC pathway, and there may be a crossover between the two pathways.