Chronic activation of vasopressin V2 receptor signalling lowers renal medullary oxygen levels in rats

Dietrich, Anja; Mathia, Susanne; Kaminski, Henriette Josephine; Mutig, Kerim; Rosenberger, Christian; Mrowka, Ralf; Bachmann, S.; Paliege, Alexander

doi:10.1111/apha.12067

Cited by 6 publications

(3 citation statements)

References 80 publications

(131 reference statements)

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“…Importantly, AVP has been shown to cause hypoxia, although only during prolonged stimulation (Dietrich et al . ).…”

Section: Renal Oxygen Consumptionmentioning

confidence: 97%

Neurohormonal interactions on the renal oxygen delivery and consumption in haemorrhagic shock-induced acute kidney injury

Hultström

2013

Acta Physiol

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Haemorrhagic shock is a common cause of acute kidney injury (AKI), which is a major risk factor for developing chronic kidney disease. The mechanism is superficially straightforward. An arterial pressure below the kidney's autoregulatory region leads to a direct reduction in filtration pressure and perfusion, which in turn cause renal failure with reduced glomerular filtration rate and AKI because of hypoxia. However, the kidney's situation is further worsened by the hormonal and neural reactions to reduced perfusion pressure. There are three major systems working to maintain arterial pressure in shock: sympathetic signalling, the renin-angiotensin system and vasopressin. These work to retain electrolytes and water and to increase peripheral resistance and cardiac output. In the kidney, the increased electrolyte reabsorption consumes oxygen. At the same time, at the signalling level seen in shock, all of these hormones reduce renal perfusion and thereby oxygen delivery. This creates an exaggerated hypoxic situation that is liable to worsen the AKI. The present review will examine this mechanistic background and identify a number of areas that require further studies. At this time, the ideal treatment of haemorrhagic shock appears to be slow fluid resuscitation, possibly with hyperosmolar sodium, low chloride and no artificial colloids. From the standpoint of the kidney, renin-angiotensin system inhibitors appear fruitful for further study.

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“…Importantly, AVP has been shown to cause hypoxia, although only during prolonged stimulation (Dietrich et al . ).…”

Section: Renal Oxygen Consumptionmentioning

confidence: 97%

Neurohormonal interactions on the renal oxygen delivery and consumption in haemorrhagic shock-induced acute kidney injury

Hultström

2013

Acta Physiol

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“…A transcriptional regulator of AQP4, miR-130a, is expressed in the brain [35], but whether a similar renal transcription factor of AQP4 is affected by dDAVP is unknown. Furthermore, long-term dDAVP administration induces renal medullary hypoxia, which upregulates hypoxia-inducible genes [36], but it is unknown how hypoxia affects the AQP4 abundance. Collectively, further studies are needed to elucidate the mechanistic basis underlying the dDAVP-induced down-regulation of AQP4 in the IMCD 2 and IMCD 3 .…”

Section: O R I G I N a L A R T I C L Ementioning

confidence: 99%

Long-term vasopressin-V2-receptor stimulation induces regulation of aquaporin 4 protein in renal inner medulla and cortex of Brattleboro rats

Poulsen

Kim

Frøkiær

et al. 2013

Nephrology Dialysis Transplantation

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“…The V2 14 receptors, which are localized in the renal collecting ducts, 15 regulate water resorption and salt (NaCl) balance. Stimulation of 16 V2 receptors by AVP reduces the urine excretion [2]. Thus, there is 17 potential to develop a AVP V2 receptor antagonist for the 18 treatment of disorders such as hyponatremia [3,4], congestive 19 heart failure [5,6], renal disease [7], edema and syndrome of 20 inappropriate antidiuretic hormone secretion (SIADH) [8].…”

mentioning

confidence: 99%

Synthesis and biological evaluation of novel phenothiazine derivatives as non-peptide arginine vasopressin V2 receptor antagonists

Zhi

Liu

et al. 2015

Chinese Chemical Letters

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Chronic activation of vasopressin V2 receptor signalling lowers renal medullary oxygen levels in rats

Abstract: Our results demonstrate that an activation of the renal urine concentrating mechanism by desmopressin causes renal medullary hypoxia and an upregulation of hypoxia-inducible gene expression.

Cited by 6 publications

References 80 publications

Neurohormonal interactions on the renal oxygen delivery and consumption in haemorrhagic shock-induced acute kidney injury

Neurohormonal interactions on the renal oxygen delivery and consumption in haemorrhagic shock-induced acute kidney injury

Long-term vasopressin-V2-receptor stimulation induces regulation of aquaporin 4 protein in renal inner medulla and cortex of Brattleboro rats

Synthesis and biological evaluation of novel phenothiazine derivatives as non-peptide arginine vasopressin V2 receptor antagonists

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