Chronic activation of plasma renin is log-linearly related to dietary sodium and eliminates natriuresis in response to a pulse change in total body sodium

Kjølby, Mads; Bie, Peter

doi:10.1152/ajpregu.00435.2007

Cited by 15 publications

(16 citation statements)

References 38 publications

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“…Recently, it was found that sodium intake determines the activity of the renin system in a log-linear fashion (441). The salt-dependent changes in the RAAS activity have been suggested to be mediated by 1) systemic humoral factors, 2) intrarenal factors, 3) renal nerves, or 4) the intrarenal MD mechanism.…”

Section: B Salt Intakementioning

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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Section: B Salt Intakementioning

confidence: 99%

Physiology of Kidney Renin

Castrop

Höcherl

Kurtz

et al. 2010

Physiological Reviews

232

277

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“…The plasma renin concentration (PRC) is log-linearly related to salt intake in humans, rats, and dogs; however, the slopes of the relationships differ [23,53,64], indicating that the salt sensitivity of the renin system differs between species. Moreover, when the results of studies in different species are compared, it should be considered that the salt intake of a rat consuming a normal laboratory diet is approximately tenfold higher than that of dogs or humans, and this intake is at the upper end of the operational range of the salt-dependent regulation of renin release [23].…”

Section: Introductionmentioning

confidence: 99%

Salt feedback on the renin-angiotensin-aldosterone system

Schweda

2014

Pflugers Arch - Eur J Physiol

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The renin-angiotensin-aldosterone system (RAAS) is a central element in the control of the salt and water balance of the body and arterial blood pressure. The activity of the RAAS is controlled by the protease renin, which is released from renal juxtaglomerular epithelioid cells (JGE cells) into the circulation. Renin release is regulated by a complex interplay of several locally acting hormones or mechanisms and longer feedback loops one of which involves salt intake. Acute NaCl loads or longer lasting high salt intakes suppress plasma renin activity, whereas reductions in NaCl intake stimulate it. Because the activation of the RAAS conserves the salt content of the body, a classical feedback loop between salt intake/body salt content and renin is established. Despite of its important role for body fluid homeostasis, the precise signaling pathways connecting salt intake with the synthesis and release of renin are only incompletely understood. Four putative controllers of the salt-dependent regulation of the RAAS have been suggested: (1) the macula densa mechanism which adjusts renin release in response to changes in the renal tubular salt concentration; (2) salt-dependent changes in the arterial blood pressure; (3) circulating salt-dependent hormones, particularly the atrial natriuretic peptide (ANP); and (4) renal sympathetic nervous activity, which is regulated by extracellular volume and arterial blood pressure. In this review, the role of these known controllers of the RAAS will be discussed with special emphasis on their relative contributions to the salt-dependent regulation of the RAAS at different time frames.

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“…In conscious dogs, a linear relationship between PRC and the logarithm of steady‐state sodium intake has been found (Kjolby et al . , Kjolby & Bie ). Similar log‐linear relationships were found for angiotensin II (ANG II) and aldosterone (Kjolby & Bie ).…”

mentioning

confidence: 96%

“…, Kjolby & Bie ). Similar log‐linear relationships were found for angiotensin II (ANG II) and aldosterone (Kjolby & Bie ). Sodium‐mediated deactivation of the RAAS occurred without changes in MABP and heart rate (HR) with a small but significant increase in plasma volume (Kjolby et al .…”

mentioning

confidence: 96%