Effects of oxytocin in normal man during low and high sodium diets

Rasmussen, Mona; Simonsen, Jørn; Sandgaard, Niels C. F.; Høilund‐Carlsen, Poul Flemming; Bie, Peter

doi:10.1111/j.1365-201x.2004.01286.x

Cited by 40 publications

(44 citation statements)

References 43 publications

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“…[17] The expression of oxytocin receptors has been shown not only in the uterine myometrium and mammary glands but also in the endometrium, decidua, ovary, thymus, pancreas, adipocytes, heart kidney, and brain. [18,19] Oxytocin plays a role in successful milk ejection, cardiovascular regulation, analgesic effects, [20] motor activity, [21] thermoregulation, [22] gastric motility, [23] natriuresis, osmoregulation, [24] and sexual behavior. It is well documented that levels of circulating oxytocin increase during sexual stimulation and arousal and peak during orgasm in both men and women.…”

Section: Discussionmentioning

confidence: 99%

Oxytocin in The Prevention of Injury Due to Testicular Torsion/Detorsion in Rats

Fırat¹,

Erdemır²,

Kölükçü³

et al. 2017

Ulus Travma Acil Cerrahi Derg

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Section: Discussionmentioning

confidence: 99%

Oxytocin in The Prevention of Injury Due to Testicular Torsion/Detorsion in Rats

Fırat¹,

Erdemır²,

Kölükçü³

et al. 2017

Ulus Travma Acil Cerrahi Derg

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“…The OT receptor antagonist atosiban attenuates the rise in PRA and heart rate in response to hydralazine or diazoxide, without affecting the blood pressure-lowering effect of these two vasodilatators (361). In contrast to these findings, the intravenous infusion of oxytocin decreased urine flow and reduced sodium excretion and PRA in humans (716). The opposite finding in humans may be due to a different expression of the renal OT receptors (35).…”

Section: Oxytocinmentioning

confidence: 99%

Physiology of Kidney Renin

Castrop

Höcherl

Kurtz

et al. 2010

Physiological Reviews

232

277

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The protease renin is the key enzyme of the renin-angiotensin-aldosterone cascade, which is relevant under both physiological and pathophysiological settings. The kidney is the only organ capable of releasing enzymatically active renin. Although the characteristic juxtaglomerular position is the best known site of renin generation, renin-producing cells in the kidney can vary in number and localization. (Pro)renin gene transcription in these cells is controlled by a number of transcription factors, among which CREB is the best characterized. Pro-renin is stored in vesicles, activated to renin, and then released upon demand. The release of renin is under the control of the cAMP (stimulatory) and Ca2+(inhibitory) signaling pathways. Meanwhile, a great number of intrarenally generated or systemically acting factors have been identified that control the renin secretion directly at the level of renin-producing cells, by activating either of the signaling pathways mentioned above. The broad spectrum of biological actions of (pro)renin is mediated by receptors for (pro)renin, angiotensin II and angiotensin-( 1 – 7 ).

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“…Levels of plasma oxytocin increase slightly in water-restricted states, concomitant with the natriuresis (2). However, oxytocin infusion in humans placed on either a high- or low-salt diet proved incapable of producing natriuresis (57).…”

Section: Sgk1 Is a Physiological Target Of Extracellular Tonicity In mentioning

confidence: 99%

Tonicity-dependent induction of Sgk1 expression has a potential role in dehydration-induced natriuresis in rodents

Chen¹,

Grigsby²,

Law³

et al. 2009

J. Clin. Invest.

199

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In various mammalian species, including humans, water restriction leads to an acute increase in urinary sodium excretion. This process, known as dehydration natriuresis, helps prevent further accentuation of hypernatremia and the accompanying rise in extracellular tonicity. Serum-and glucocorticoid-inducible kinase (Sgk1), which is expressed in the renal medulla, is regulated by extracellular tonicity. However, the mechanism of its regulation and the physiological role of hypertonicity-induced SGK1 gene expression remain unclear. Here, we identified a tonicity-responsive enhancer (TonE) upstream of the rat Sgk1 transcriptional start site. The transcription factor NFAT5 associated with TonE in a tonicity-dependent fashion in cultured rat renal medullary cells, and selective blockade of NFAT5 activity resulted in suppression of the osmotic induction of the Sgk1 promoter. In vivo, water restriction of rats or mice led to increased urine osmolality, increased Sgk1 expression, increased expression of the type A natriuretic peptide receptor (NPR-A), and dehydration natriuresis. In cultured rat renal medullary cells, siRNA-mediated Sgk1 knockdown blocked the osmotic induction of natriuretic peptide receptor 1 (Npr1) gene expression. Furthermore, Npr1 -/-mice were resistant to dehydration natriuresis, which suggests that Sgk1-dependent activation of the NPR-A pathway may contribute to this response. Collectively, these findings define a specific mechanistic pathway for the osmotic regulation of Sgk1 gene expression and suggest that Sgk1 may play an important role in promoting the physiological response of the kidney to elevations in extracellular tonicity. IntroductionPersistent hypertonicity, typically reflecting a high extracellular sodium concentration, stresses mammalian cells due to the ensuing osmotic efflux of water that shrinks the cells and concentrates their contents. Under most conditions, the concentration of extracellular sodium in mammals is controlled primarily through regulation of water metabolism. As extracellular sodium and plasma tonicity rise, the thirst mechanism is activated, and secretion of the neurohypophyseal hormone vasopressin into plasma increases. Vasopressin binds to its cognate receptors in the collecting duct of the kidney, resulting in increased water retention.Following short-term water restriction, several mammals demonstrate an acute increase in urinary sodium excretion that is independent of changes in water metabolism. This response, termed dehydration natriuresis (1-11), plays an important role in preventing further accentuation of hypernatremia and the accompanying rise in extracellular tonicity. A similar natriuresis is seen following infusion of hypertonic saline (12). Investigations to date have suggested a role for central versus peripheral osmoreceptors and blood-borne versus neural effectors in contributing to dehydration-induced natriuresis; however, the precise mechanism(s) underlying this natriuresis remains undefined.

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Effects of oxytocin in normal man during low and high sodium diets

Cited by 40 publications

References 43 publications

Oxytocin in The Prevention of Injury Due to Testicular Torsion/Detorsion in Rats

Oxytocin in The Prevention of Injury Due to Testicular Torsion/Detorsion in Rats

Physiology of Kidney Renin

Tonicity-dependent induction of Sgk1 expression has a potential role in dehydration-induced natriuresis in rodents

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