Vasopressin and Breathing: Review of Evidence for Respiratory Effects of the Antidiuretic Hormone

Vasopressin (AVP) is a key neurohormone involved in the regulation of body functions. Due to its urine-concentrating effect in the kidneys, it is often referred to as antidiuretic hormone. Besides its antidiuretic renal effects, AVP is a potent neurohormone involved in the regulation of arterial blo...

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Autores principales: Michał Proczka, Jacek Przybylski, Agnieszka Cudnoch-Jędrzejewska, Ewa Szczepańska-Sadowska, Tymoteusz Żera
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Publicado: Frontiers Media S.A. 2021
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spelling oai:doaj.org-article:f95f5da44c4b42b088ca2f0e0932e4f42021-11-16T18:42:18ZVasopressin and Breathing: Review of Evidence for Respiratory Effects of the Antidiuretic Hormone1664-042X10.3389/fphys.2021.744177https://doaj.org/article/f95f5da44c4b42b088ca2f0e0932e4f42021-10-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fphys.2021.744177/fullhttps://doaj.org/toc/1664-042XVasopressin (AVP) is a key neurohormone involved in the regulation of body functions. Due to its urine-concentrating effect in the kidneys, it is often referred to as antidiuretic hormone. Besides its antidiuretic renal effects, AVP is a potent neurohormone involved in the regulation of arterial blood pressure, sympathetic activity, baroreflex sensitivity, glucose homeostasis, release of glucocorticoids and catecholamines, stress response, anxiety, memory, and behavior. Vasopressin is synthesized in the paraventricular (PVN) and supraoptic nuclei (SON) of the hypothalamus and released into the circulation from the posterior lobe of the pituitary gland together with a C-terminal fragment of pro-vasopressin, known as copeptin. Additionally, vasopressinergic neurons project from the hypothalamus to the brainstem nuclei. Increased release of AVP into the circulation and elevated levels of its surrogate marker copeptin are found in pulmonary diseases, arterial hypertension, heart failure, obstructive sleep apnoea, severe infections, COVID-19 due to SARS-CoV-2 infection, and brain injuries. All these conditions are usually accompanied by respiratory disturbances. The main stimuli that trigger AVP release include hyperosmolality, hypovolemia, hypotension, hypoxia, hypoglycemia, strenuous exercise, and angiotensin II (Ang II) and the same stimuli are known to affect pulmonary ventilation. In this light, we hypothesize that increased AVP release and changes in ventilation are not coincidental, but that the neurohormone contributes to the regulation of the respiratory system by fine-tuning of breathing in order to restore homeostasis. We discuss evidence in support of this presumption. Specifically, vasopressinergic neurons innervate the brainstem nuclei involved in the control of respiration. Moreover, vasopressin V1a receptors (V1aRs) are expressed on neurons in the respiratory centers of the brainstem, in the circumventricular organs (CVOs) that lack a blood-brain barrier, and on the chemosensitive type I cells in the carotid bodies. Finally, peripheral and central administrations of AVP or antagonists of V1aRs increase/decrease phrenic nerve activity and pulmonary ventilation in a site-specific manner. Altogether, the findings discussed in this review strongly argue for the hypothesis that vasopressin affects ventilation both as a blood-borne neurohormone and as a neurotransmitter within the central nervous system.Michał ProczkaJacek PrzybylskiAgnieszka Cudnoch-JędrzejewskaEwa Szczepańska-SadowskaTymoteusz ŻeraFrontiers Media S.A.articleantidiuretic hormonerespirationcardiovascular systemcarotid bodysympathetic nervous systemcircumventricular organsPhysiologyQP1-981ENFrontiers in Physiology, Vol 12 (2021)
institution DOAJ
collection DOAJ
language EN
topic antidiuretic hormone
respiration
cardiovascular system
carotid body
sympathetic nervous system
circumventricular organs
Physiology
QP1-981
spellingShingle antidiuretic hormone
respiration
cardiovascular system
carotid body
sympathetic nervous system
circumventricular organs
Physiology
QP1-981
Michał Proczka
Jacek Przybylski
Agnieszka Cudnoch-Jędrzejewska
Ewa Szczepańska-Sadowska
Tymoteusz Żera
Vasopressin and Breathing: Review of Evidence for Respiratory Effects of the Antidiuretic Hormone
description Vasopressin (AVP) is a key neurohormone involved in the regulation of body functions. Due to its urine-concentrating effect in the kidneys, it is often referred to as antidiuretic hormone. Besides its antidiuretic renal effects, AVP is a potent neurohormone involved in the regulation of arterial blood pressure, sympathetic activity, baroreflex sensitivity, glucose homeostasis, release of glucocorticoids and catecholamines, stress response, anxiety, memory, and behavior. Vasopressin is synthesized in the paraventricular (PVN) and supraoptic nuclei (SON) of the hypothalamus and released into the circulation from the posterior lobe of the pituitary gland together with a C-terminal fragment of pro-vasopressin, known as copeptin. Additionally, vasopressinergic neurons project from the hypothalamus to the brainstem nuclei. Increased release of AVP into the circulation and elevated levels of its surrogate marker copeptin are found in pulmonary diseases, arterial hypertension, heart failure, obstructive sleep apnoea, severe infections, COVID-19 due to SARS-CoV-2 infection, and brain injuries. All these conditions are usually accompanied by respiratory disturbances. The main stimuli that trigger AVP release include hyperosmolality, hypovolemia, hypotension, hypoxia, hypoglycemia, strenuous exercise, and angiotensin II (Ang II) and the same stimuli are known to affect pulmonary ventilation. In this light, we hypothesize that increased AVP release and changes in ventilation are not coincidental, but that the neurohormone contributes to the regulation of the respiratory system by fine-tuning of breathing in order to restore homeostasis. We discuss evidence in support of this presumption. Specifically, vasopressinergic neurons innervate the brainstem nuclei involved in the control of respiration. Moreover, vasopressin V1a receptors (V1aRs) are expressed on neurons in the respiratory centers of the brainstem, in the circumventricular organs (CVOs) that lack a blood-brain barrier, and on the chemosensitive type I cells in the carotid bodies. Finally, peripheral and central administrations of AVP or antagonists of V1aRs increase/decrease phrenic nerve activity and pulmonary ventilation in a site-specific manner. Altogether, the findings discussed in this review strongly argue for the hypothesis that vasopressin affects ventilation both as a blood-borne neurohormone and as a neurotransmitter within the central nervous system.
format article
author Michał Proczka
Jacek Przybylski
Agnieszka Cudnoch-Jędrzejewska
Ewa Szczepańska-Sadowska
Tymoteusz Żera
author_facet Michał Proczka
Jacek Przybylski
Agnieszka Cudnoch-Jędrzejewska
Ewa Szczepańska-Sadowska
Tymoteusz Żera
author_sort Michał Proczka
title Vasopressin and Breathing: Review of Evidence for Respiratory Effects of the Antidiuretic Hormone
title_short Vasopressin and Breathing: Review of Evidence for Respiratory Effects of the Antidiuretic Hormone
title_full Vasopressin and Breathing: Review of Evidence for Respiratory Effects of the Antidiuretic Hormone
title_fullStr Vasopressin and Breathing: Review of Evidence for Respiratory Effects of the Antidiuretic Hormone
title_full_unstemmed Vasopressin and Breathing: Review of Evidence for Respiratory Effects of the Antidiuretic Hormone
title_sort vasopressin and breathing: review of evidence for respiratory effects of the antidiuretic hormone
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/f95f5da44c4b42b088ca2f0e0932e4f4
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