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.

Highlights

  • Foreword: This review is the result of a didactic project at Concordia University in Montreal employing a novel “write to learn” pedagogy [1] that we have used successfully before [2,3]

  • We review the biology of arginine vasopressin (AVP) through examination of its normal physiological roles in the kidneys and heart, its neurological and behavioral effects, how AVP dysfunction contributes to pathologies such as polycystic kidney disease (PKD), heart failure (HF), neuropsychiatric disorders, and the pharmacological manipulation of AVP-dependent pathways

  • Other AVP-synthesizing neurons can be found in the medial amygdala, the bed nucleus of the stria terminalis (BNST), and the Suprachiasmatic nucleus (SCN), which all project centrally to the brain preoptic and olfactory areas, hypothalamic, and extra-hypothalamic regions [54,176,177,178]

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Summary

Introduction

Foreword: This review is the result of a didactic project at Concordia University in Montreal employing a novel “write to learn” pedagogy [1] that we have used successfully before [2,3]. Senior undergraduate students enrolled in a Comparative Physiology course for third-year Biology majors were taught experientially how to research and study the scientific literature to write a collaborative analytical review on the biological activity of vasopressin. AVP Function AVP secretion from the posterior pituitary is triggered by changes in the electrolytewater balance affecting intravascular blood volume and osmolality, that respectively activate baroreceptors [20] and osmoreceptors [21]. Changes in osmolality of the thalamic magnocellular cells activate nonselective cation channels, increase the action potentials firing rate, and trigger AVP release from axon terminals ([23], reviewed in [24]). Pro-AVP is stored in membrane-associated granules and released in response to increased extracellular fluid osmolarity and osmoreceptor activation [25]. AVP circulates as a free hormone and is degraded enzymatically in the liver and kidney within 10–30 min of release [49]

AVP Receptors
Kidney
Biological Sex and PKD
AVP and Heart Failure
AVP-V1aR Signaling and Cardiac Contractility
AVP-V1aR Signaling and Cardiac Remodeling
AVP-V2R Signaling for Fluid Volume Retention and Cardiac Function
AVP and Brain Function
AVP and Animal Behavior
V1bR and Behavior
Circadian Response
AVP and Human Behaviour
Pharmacological Modulation of the AVP Pathways
Vasopressin Receptor Antagonists
Clinical Trials
Synthetic AVP Analogs
Findings
Conclusions
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