Vasopressin V1a receptors are present in the carotid body and contribute to the control of breathing in male Sprague-Dawley rats

Żera, Tymoteusz; Przybylski, Jacek; Grygorowicz, Tomasz; Kasarełło, Kaja; Podobińska, Martyna; Mirowska‐Guzel, Dagmara; Cudnoch-Jędrzejewska, Agnieszka

doi:10.1016/j.peptides.2018.03.004

Cited by 13 publications

(15 citation statements)

References 38 publications

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“…7,8 These findings were corroborated by experiments in another species, namely Sprague-Dawley rats. 9 Therefore, in our patients with ADPKD, it could be that as result of V2 blockade, vasopressin increases, thereby activating more V1 receptors and thus resulting in a decreased respiratory rate and decreased pCO 2 . Although it certainly can be debated whether the venous pCO2 is a reliable reflection of its arterial value, the significant decrease in paired measurements of this arguably variable measure in this small cohort, together with the theoretical rationale, make this hypothesis more convincing.…”

mentioning

confidence: 81%

Acid-Base Homeostasis During Vasopressin V2 Receptor Antagonist Treatment in Autosomal Dominant Polycystic Kidney Disease Patients

Heida

Gansevoort

Meijer

2021

Kidney International Reports

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mentioning

confidence: 81%

Acid-Base Homeostasis During Vasopressin V2 Receptor Antagonist Treatment in Autosomal Dominant Polycystic Kidney Disease Patients

Heida

Gansevoort

Meijer

2021

Kidney International Reports

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“…Vasopressinergic PVN neurons project to cardiovascular (RVLM) and respiratory (preBC/BC, rVRG, and C4 phrenic nucleus) centers, suggesting their involvement in the respiratory control ( Kc et al, 2002a , 2010 ). (1) AVP at the AP inhibits phrenic nerve activity ( Yang et al, 2006 ); (2) vasopressinergic projections to the rVRG tonically stimulate respiratory activity ( Kc et al, 2010 ) and AVP applied into the rVRG or pre-Bötzinger complex stimulates activity of diaphragm ( Kc et al, 2002a , 2010 ), which is accompanied by increase in arterial blood pressure; this is in contrast to findings indicating that AVP administered into the rVRG inhibits phrenic nerve activity with and without changes in arterial blood pressure ( Chuang et al, 2003 , 2005 ; Cheng et al, 2004 ); (3) AVP locally administered into the carotid bifurcation slightly increases ventilation ( Żera et al, 2018 ); and (4) vasopressin receptors are expressed in the SFO ( Ostrowski et al, 1994 ), and electric stimulation of SFO increases respiratory activity ( Ferguson et al, 1989 ), but the respiratory effects of AVP acting at SFO have not been determined. AP, area postrema; AVP, vasopressin; BC, Bötzinger complex; C4, phrenic nuclei; CVLM, caudal ventrolateral medulla; cVRG, caudal ventral respiratory group; NTS, nucleus of the solitary tract; OVLT, organum vasculosum of the lamina terminalis; preBC, pre-Bötzinger complex; PVN, paraventricular nucleus of the hypothalamus; RVLM, rostral ventrolateral medulla; rVRG, rostral ventral respiratory group; SFO, subfornical organ; SON, supraoptic nucleus; and VLM, ventral lateral medulla.…”

Section: Physiology Of Vasopressinmentioning

confidence: 97%

“…Available evidence indicates that its respiratory effects are mainly mediated by V1aRs. Vasopressin present in the bloodstream may affect the respiratory system by interacting with V1aRs expressed in the lungs ( Tahara et al, 1998 ), the circumventricular organs (CVOs; Raggenbass et al, 1989 ; Ostrowski et al, 1994 ; Tribollet et al, 1999 ; Hindmarch et al, 2011 ), and in the carotid bodies ( Żera et al, 2018 ). In addition to circulating AVP, vasopressinergic neurons projecting to the brainstem respiratory centers affect respiratory activity via V1aRs ( Kc et al, 2002a , 2010 ; Chuang et al, 2005 ; Kc and Dick, 2010 ).…”

Section: The Respiratory Effects Of Vasopressinmentioning

confidence: 99%

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

et al. 2021

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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.

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“…Experiments have made it possible to detect V1aR, V1bR, and OXTR mRNAs and proteins in the cerebral cortex, hypothalamus, pons, medulla, and cerebellum [ 3 , 29 , 33 , 50 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 ]. V1R and OXTR are also present in the arteries, veins, heart, lungs, carotid bodies, kidneys, adrenal glands, pancreas, gastrointestinal tract, eyes, ovaries, uterus, thymus, and autonomic ganglia [ 30 , 35 , 37 , 38 , 46 , 69 , 73 , 74 , 75 , 76 , 77 , 78 ]. Vasopressin V2R mRNA and protein were found in the kidneys and the urinary bladder [ 58 , 79 , 80 ].…”

Section: Vasopressin and Oxytocin Receptorsmentioning

confidence: 99%

Complementary Role of Oxytocin and Vasopressin in Cardiovascular Regulation

Szczepañska‐Sadowska

Wsol

Cudnoch-Jędrzejewska

et al. 2021

IJMS

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The neurons secreting oxytocin (OXY) and vasopressin (AVP) are located mainly in the supraoptic, paraventricular, and suprachiasmatic nucleus of the brain. Oxytocinergic and vasopressinergic projections reach several regions of the brain and the spinal cord. Both peptides are released from axons, soma, and dendrites and modulate the excitability of other neuroregulatory pathways. The synthesis and action of OXY and AVP in the peripheral organs (eye, heart, gastrointestinal system) is being investigated. The secretion of OXY and AVP is influenced by changes in body fluid osmolality, blood volume, blood pressure, hypoxia, and stress. Vasopressin interacts with three subtypes of receptors: V1aR, V1bR, and V2R whereas oxytocin activates its own OXTR and V1aR receptors. AVP and OXY receptors are present in several regions of the brain (cortex, hypothalamus, pons, medulla, and cerebellum) and in the peripheral organs (heart, lungs, carotid bodies, kidneys, adrenal glands, pancreas, gastrointestinal tract, ovaries, uterus, thymus). Hypertension, myocardial infarction, and coexisting factors, such as pain and stress, have a significant impact on the secretion of oxytocin and vasopressin and on the expression of their receptors. The inappropriate regulation of oxytocin and vasopressin secretion during ischemia, hypoxia/hypercapnia, inflammation, pain, and stress may play a significant role in the pathogenesis of cardiovascular diseases.

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Vasopressin V1a receptors are present in the carotid body and contribute to the control of breathing in male Sprague-Dawley rats

Cited by 13 publications

References 38 publications

Acid-Base Homeostasis During Vasopressin V2 Receptor Antagonist Treatment in Autosomal Dominant Polycystic Kidney Disease Patients

Acid-Base Homeostasis During Vasopressin V2 Receptor Antagonist Treatment in Autosomal Dominant Polycystic Kidney Disease Patients

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

Complementary Role of Oxytocin and Vasopressin in Cardiovascular Regulation

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