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Trial to control the formation of endolymphatic hydrops from the viewpoint of the water homeostasis of the inner ear. | LitMetric

Trial to control the formation of endolymphatic hydrops from the viewpoint of the water homeostasis of the inner ear.

Auris Nasus Larynx

Department of Otolaryngology-Head & Neck Surgery, Kobe University, Graduate School of Medicine, Hyogo, Japan. Electronic address:

Published: April 2025

Endolymphatic hydrops, which is one of the pathologic features of Ménière's disease, has been experimentally and clinically confirmed to be influenced by the blood circulation of vasopressin (VP). It is widely acknowledged that VP plays a pivotal role in regulating water homeostasis. It should also be noted that VP is susceptible to a number of external factors, including changes in the environment, dehydration, and fluctuations in atmospheric pressure. Furthermore, VP is a key regulator of the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis is a significant neuroendocrine system that plays a role in regulating responses to emotional and physical stress, as well as the sleep/wake cycle (circadian rhythm). It seems that VP is changeable via the HPA axis. It may be beneficial to consider pharmacological normalization of VP as a potential approach to controlling Ménière's disease. Nevertheless, measuring 8-Arg-vasopressin (AVP), the most prevalent variant of VP, poses certain challenges for a number of reasons. Copeptin is co-released with AVP, is relatively stable in the posterior pituitary as well as in blood plasma, and is increasingly being used as an AVP surrogate in clinical diagnostics. It is thought that the use of copeptin as a marker for AVP may help to clarify the clinical features of Ménière's disease. In this review, we will consider trials to control the formation of endolymphatic hydrops from the viewpoint of the vasopressin-aquaporin 2 system. Furthermore, we will explore reports on clinical treatment, pharmacological agents, and future prospects.

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http://dx.doi.org/10.1016/j.anl.2025.01.001DOI Listing

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