AVPR1B is responsible for fueling the effects of vasopressin on ACTH release. This interaction takes place as Arginine Vasopressin works with corticotropin releasing hormone to stimulate the pituitary gland to secrete ACTH. AVPR1b is then responsible for mediating the stimulatory effect of vasopressin on ACTH release. Several G proteins are also involved in the signal transduction pathways linked with AVPR1B. These relationships depend on the level of receptor expression and concentration of vasopressin. For example, AVPR1B causes secretion of ACTH from the anterior pituitary cells in a dose-dependent relationship by activating protein kinase C via the Gq/11 protein. Application There have been several experiments which have studied these interactions further and revealed AVPR1B's role in psychological disorders and regulatory functions. Haplotypes of AVPR1B are associated with increased protective effects to recurrent major depression. AVPR1B has also been associated with higher cortisol responses to psychosocial stress in children with psychiatric disorders compared with carriers of glucocorticoid receptor gene. AVPR1b has also shown involvement in regulation of brain water content and cerebral edema. This was revealed as increased levels of AVPR1B mRNA on the choroid plexus were discovered as a result of increased plasma osmolality. The increase after a reduction of brain water content from salt water loading indicated AVPR1B's role in the neuroendocrine feedback loop in maintaining normal central nervous system fluid balance. References External links G protein-coupled receptors