The Biology of Vasopressin

Abstract

Vasopressins are evolutionarily conserved peptide hormones. Mammalian vasopressin functions systemically as an antidiuretic and regulator of blood and cardiac flow essential for adapting to terrestrial environments. Moreover, vasopressin acts centrally as a neurohormone involved in social and parental behavior and stress response. Vasopressin synthesis in several cell types, storage in intracellular vesicles, and release in response to physiological stimuli are highly regulated and mediated by three distinct G protein coupled receptors. Other receptors may bind or cross-bind vasopressin. Vasopressin is regulated spatially and temporally through transcriptional and post-transcriptional mechanisms, sex, tissue, and cell-specific receptor expression. Anomalies of vasopressin signaling have been observed in polycystic kidney disease, chronic heart failure, and neuropsychiatric conditions. Growing knowledge of the central biological roles of vasopressin has enabled pharmacological advances to treat these conditions by targeting defective systemic or central pathways utilizing specific agonists and antagonists.

Effect of Vasopressin and its Analogs versus Catecholamines on the Renal Outcomes in Septic Shock:A Systematic Review and Meta-Analysis of Randomized Trials

“…Catecholamines like Norepinephrine reduces urine ow by preferentially binding to α1-adrenoreceptors, mainly located on renal afferent arterioles, contributing to decreased glomerular ltration rate (GFR), creatinine clearance, and urine output (40,41). In contrast, Vasopressin results in increased urine output and improved glomerular ltration rate by binding to V1a receptors on efferent glomerular arterioles without constricting afferent arterioles (41)(42)(43).…”

Modeling Neoplastic Growth in Renal Cell Carcinoma and Polycystic Kidney Disease

“…In addition to contributing to cystic growth, ADPKD upsets polarization of the tubular epithelium. Increased fluid secretion in early disease stage triggers compensatory vasopressin release and systemic responses affecting the cardiovascular system (reviewed in [35]). Moreover, ADPKD patients suffer from several extra-renal manifestations (reviewed in [34]).…”

“…Concurrent c-Myc upregulation promotes cell proliferation and, together with increased Bcl-2 expression and reduced p53 protein levels, also dysregulates apoptosis [107,108]. The V2R signaling cascade becomes progressively upregulated in ADPKD, which raises intracellular cAMP levels and characteristically contributes to cystic cell growth and proliferation (reviewed in [35]). Of note, in normal renal epithelial cells, high cAMP levels inhibit cell proliferation (reviewed in [109]).…”

Potential Use of Pharmacogenetics to Reduce Drug-Induced Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

“…They are structurally and functionally distinct from the glandular tissue of the anterior pituitary gland (the adenohypophysis). When serum sodium levels rise above 145 mEq/L, hypothalamic osmoreceptors located in the supraoptic and paraventricular nuclei activate secretion of ADH directly from the posterior pituitary [ 14 ] ( Figure 1 A). The resulting increase in systemic levels of ADH then leads to enhanced water reabsorption by the kidneys.…”