Insulin‐like growth factor I administration induces fluid and sodium retention in healthy adults: possible involvement of renin and atrial natriuretic factor

Møller, Jens Kjølseth; Jørgensen, Jens O. L.; Marqversen, J.; Frandsen, Erik; Christiansen, Jens Sandahl

doi:10.1046/j.1365-2265.2000.00931.x

Cited by 45 publications

(41 citation statements)

References 38 publications

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“…It has been suggested that several effects of GH are at least partly mediated by insulin-like growth factor I (IGF-I) (591). Indeed, it has been found that IGF-I increases PRA in rats and fetal sheep and stimulates the secretion of renin from renal cortical slices (392,408,563,564), but the precise role of IGF-I for GH-induced renin release is unknown.…”

Section: Growth Hormone and Insulin-like Growth Factor Imentioning

confidence: 99%

Physiology of Kidney Renin

Castrop

Höcherl

Kurtz

et al. 2010

Physiological Reviews

234

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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Section: Growth Hormone and Insulin-like Growth Factor Imentioning

confidence: 99%

Physiology of Kidney Renin

Castrop

Höcherl

Kurtz

et al. 2010

Physiological Reviews

234

277

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“…IGF-1 production is under strict control of growth hormone (GH). GH infusion to healthy humans increases renal IGF-1 production and stimulates renal Na + and fluid transport [125,133,222] which has been used to explain that patients with acromegaly (GH over-production) frequently develop arterial hypertension [36]. Recently, Kamenicky and coworkers studied acromegalic GC rats to analyse the molecular mechanism responsible for renal Na + retention in these rats.…”

Section: Regulation Of Enac By Insulin/igf-1mentioning

confidence: 99%

Regulated sodium transport in the renal connecting tubule (CNT) via the epithelial sodium channel (ENaC)

Loffing

Korbmacher

2009

Pflugers Arch - Eur J Physiol

147

141

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The aldosterone-sensitive distal nephron (ASDN) includes the late distal convoluted tubule 2, the connecting tubule (CNT) and the collecting duct. The appropriate regulation of sodium (Na + ) absorption in the ASDN is essential to precisely match urinary Na + excretion to dietary Na + intake whilst taking extra-renal Na + losses into account. There is increasing evidence that Na + transport in the CNT is of particular importance for the maintenance of body Na + balance and for the long-term control of extracellular fluid volume and arterial blood pressure. Na + transport in the CNT critically depends on the activity and abundance of the amiloride-sensitive epithelial sodium channel (ENaC) in the luminal membrane of the CNT cells. As a rate-limiting step for transepithelial Na + transport, ENaC is the main target of hormones (e.g. aldosterone, angiotensin II, vasopressin and insulin/insulinlike growth factor 1) to adjust transepithelial Na + transport in this tubular segment. In this review, we highlight the structural and functional properties of the CNT that contribute to the high Na + transport capacity of this segment. Moreover, we discuss some aspects of the complex pathways and molecular mechanisms involved in ENaC regulation by hormones, kinases, proteases and associated proteins that control its function. Whilst cultured cells and heterologous expression systems have greatly advanced our knowledge about some of these regulatory mechanisms, future studies will have to determine the relative importance of the various pathways in the native tubule and in particular in the CNT.

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“…In addition to the direct effects of GH and IGF-1 on the vasculature, several other pathophysiological mechanisms have been postulated to contribute to hypertension in acromegaly [18], including GH-mediated increased renal tubular sodium reabsorption [19] and inhibition of atrial natriuretic peptide by IGF-1 [20]. Where present, elevated insulin levels may also lead to increased sodium reabsorption with activation of the renin-angiotensin-aldosterone system.…”

Section: Cardiovascular Complicationsmentioning

confidence: 99%

Cardiovascular Disease and Sleep-Disordered Breathing in Acromegaly

Powlson

Gurnell²

2015

Neuroendocrinology

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Treatment goals in acromegaly include symptom relief, tumour control and reversal of the excess morbidity and mortality associated with the disorder. Cardiovascular complications include concentric biventricular hypertrophy and cardiomyopathy, hypertension, valvular heart disease and arrhythmias, while metabolic disturbance (insulin resistance/diabetes mellitus, dyslipidaemia) further increases the risk of cardiovascular and cerebrovascular events. Sleep-disordered breathing (in the form of sleep apnoea) is also common in patients with acromegaly and may exacerbate cardiovascular dysfunction, in addition to contributing to impaired quality of life. Accordingly, and in keeping with evidence that cardiorespiratory complications in acromegaly are not automatically reversed/ameliorated simply through the attainment of ‘safe' growth hormone and insulin-like growth factor 1 levels, recent guidelines have emphasised the need not only to achieve stringent biochemical control, but also to identify and independently treat these comorbidities. It is important, therefore, that patients with acromegaly are systematically screened at diagnosis, and periodically thereafter, for the common cardiovascular and respiratory manifestations and that biochemical targets do not become the only treatment goal.

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Insulin‐like growth factor I administration induces fluid and sodium retention in healthy adults: possible involvement of renin and atrial natriuretic factor

Abstract: IGF-I treatment causes fluid and sodium retention. This may be mediated by increased renin release and suppression of atrial natriuretic factor. The present data suggest that the fluid and sodium retaining effect of GH is at least partly mediated through IGF-I.

Cited by 45 publications

References 38 publications

Physiology of Kidney Renin

Physiology of Kidney Renin

Regulated sodium transport in the renal connecting tubule (CNT) via the epithelial sodium channel (ENaC)

Cardiovascular Disease and Sleep-Disordered Breathing in Acromegaly

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