Salt sensitivity of renin secretion, glomerular filtration rate and blood pressure in conscious <scp>S</scp>prague‐<scp>D</scp>awley rats

Isaksson, Gustaf Lissel; Stubbe, Jane; Hansen, Per Lyngs; Jensen, Boye L.; Bie, Peter

doi:10.1111/apha.12191

Cited by 15 publications

(18 citation statements)

References 36 publications

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“…54, 60 Of note, a recent study found GFR to be NaCl-sensitive. 61 All NHE3 loxloxCre mice and Con mice in this study clearly respond to low NaCl intake with a reduction in GFR, possibly indicating intact resetting of the TGF response in order to restore efficiency. 62 The reduced GFR in NHE3 loxloxCre mice is possibly another mechanism that contributes to the maintenance of NaCl homeostasis.…”

Section: Discussionmentioning

confidence: 65%

Renal tubular NHE3 is required in the maintenance of water and sodium chloride homeostasis

Fenton

Poulsen

Chavez

et al. 2017

Kidney International

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The sodium/proton exchanger isoform 3 (NHE3) is expressed in the intestine and the kidney where it facilitates sodium (re)absorption and proton secretion. The importance of NHE3 in the kidney for sodium chloride homeostasis, relative to the intestine, is unknown. Constitutive tubule-specific NHE3 knockout mice (NHE3loxloxCre) did not show significant differences compared to control mice in body weight, blood pH or bicarbonate and plasma sodium, potassium or aldosterone levels. Fluid intake, urinary flow rate, urinary sodium/creatinine and pH were significantly elevated in NHE3loxloxCre mice while urine osmolality and GFR were significantly lower. Water deprivation revealed a small urinary concentrating defect in NHE3loxloxCre mice on a control diet; exaggerated on low sodium chloride. Ten days of low or high sodium chloride diet did not affect plasma sodium in control mice; however, NHE3loxloxCre mice were susceptible to low sodium chloride (about −4 mM) or high sodium chloride intake (about +2 mM) versus baseline, effects without differences in plasma aldosterone between groups. Blood pressure was significantly lower in NHE3loxloxCre mice and was sodium chloride-sensitive. In control mice, the expression of the sodium/phosphate co-transporter Npt2c was sodium chloride-sensitive. However, lack of tubular NHE3 blunted Npt2c expression. Alterations in the abundances of sodium/chloride cotransporter and its phosphorylation at threonine 58 as well as the abundances of the α-subunit of the epithelial sodium channel, and its cleaved form, were also apparent in NHE3loxloxCre mice. Thus, renal NHE3 is required to maintain blood pressure and steady state plasma sodium levels when dietary sodium chloride intake is modified.

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Section: Discussionmentioning

confidence: 65%

Renal tubular NHE3 is required in the maintenance of water and sodium chloride homeostasis

Fenton

Poulsen

Chavez

et al. 2017

Kidney International

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“…Whereas acute maneuvers will affect the release of renin from preformed mature renin vesicles, long-term changes in salt intake will also regulate renin synthesis and expression. In response to intravenous salt loading, PRC fell with a half life of 4.6 h, whereas renal renin mRNA expression did not change over the experimental period of 48 h [53]. During longer lasting reductions of salt intake, the number of reninproducing cells increases by a reversible transformation of preglomerular vascular smooth muscle cells into reninproducing cells (Fig.…”

Section: Introductionmentioning

confidence: 87%

“…A general stimulatory role of renal sympathetic nerve activity has been shown by pharmacological blockade of ß1-receptors, renal denervation, and genetic deletion of both ß1-and ß2-receptors (ß1/ß2 double knockout mice), which all significantly reduced the renin synthesis and/or plasma renin levels under control conditions [18,26,37,50,58,82]. In some but not all studies, renal denervation or ß-receptor blockade affected the saltdependent regulation of the renin system such that the absolute levels of renal renin mRNA expression and plasma renin activity were lower under low or high salt load compared with those in the animals or humans with intact renal efferent inputs [47,49,53,82,96,119]. Notably, the salt-dependent regulation of the renin system was not abrogated in any of these studies, and the relative stimulation of the renin system, which was calculated as the stimulation relative to baseline values under normal salt intake, was maintained in the absence of renal ß-adrenergic innervation [82].…”

Section: Renal Sympathetic Nerve Activitymentioning

confidence: 99%

“…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%

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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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“…) regulate sodium balance (reviewed in: Isaksson et al . ). Therein, the kidneys play a major role, embedded in an intricate and interwoven network of electrolyte and blood pressure regulation mechanisms (Healy et al .…”

mentioning

confidence: 97%

Salt: a matter of balance

Persson

2016

Acta Physiol

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Salt sensitivity of renin secretion, glomerular filtration rate and blood pressure in conscious Sprague‐Dawley rats

Cited by 15 publications

References 36 publications

Renal tubular NHE3 is required in the maintenance of water and sodium chloride homeostasis

Renal tubular NHE3 is required in the maintenance of water and sodium chloride homeostasis

Salt feedback on the renin-angiotensin-aldosterone system

Salt: a matter of balance

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