Resetting of tubulo-glomerular feedback sensitivity by dietary salt intake

B, Dev; Drescher, Caitlin; Schnermann, Jürgen

doi:10.1007/bf00596182

Cited by 64 publications

(19 citation statements)

References 31 publications

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“…Some experiments have indicated that tubular fluid osmolality may also regulate the nephron feedback response although this remains controversial (4,43). "Feedback inhibition" of SNGFR occurs during infusion of hypertonic NaCl but not hypertonic NaHCO3 (44), is augmented by prior dietary salt restriction (45), and is independent of the nervous system (46). In one series, feedback inhibition of SNGFR was accompanied by a rise in FF (47) but in a recent study, Ichikawa has shown that although feedback inhibition of SNGFR is accompanied by comparable increases in afferent and efferent arteriolar resistance, the FF falls because SNGFR is reduced not only by the fall in plasma flow rate, but also by a large fall in the glomerular capillary ultrafiltration coefficient (39).…”

Section: Experimental Protocolmentioning

confidence: 99%

“…To define the separate effects of an acute increase in plasma sodium (PNa), chloride (Pci) or osmolality (Posmoi), changes in renal blood flow (RBF) and GFR were measured during intrarenal infusions of hypertonic NaCl, NaHCO3, Na acetate, dextrose, NH4Cl or NH4acetate to denervated kidneys. The infusions raised Posmol at the experimental kidney by [30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45] mosmol. RBF increased abruptly by 10-30% with all hypertonic infusions indicating that an acute increase in plasma tonicity causes renal vasodilatation.…”

mentioning

confidence: 99%

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Regulation of Renal Blood Flow by Plasma Chloride

Wilcox¹

1983

J. Clin. Invest.

599

340

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A B S T R A C T Micropuncture studies have shown that glomerular filtration rate (GFR) falls in response to a rise in Na' or Cl-concentrations in the loop of Henle, whereas studies in isolated kidneys have shown that GFR falls in response to osmotic diuresis. To define the separate effects of an acute increase in plasma sodium (PNa), chloride (Pci) or osmolality (Posmoi), changes in renal blood flow (RBF) and GFR were measured during intrarenal infusions of hypertonic NaCl, NaHCO3, Na acetate, dextrose, NH4Cl or NH4acetate to denervated kidneys. The infusions raised Posmol at the experimental kidney by [30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45] mosmol. RBF increased abruptly by 10-30% with all hypertonic infusions indicating that an acute increase in plasma tonicity causes renal vasodilatation. Renal vasodilatation persisted or increased further during infusion of dextrose, NaHCO3 and Na acetate, but GFR was unchanged. In contrast, during infusion of the two Clcontaining solutions, vasodilatation was reversed after 1-5 min and RBF and GFR decreased (P < 0.01) below preinfusion levels. Prior salt depletion doubled the vasoconstriction seen with hypertonic NaCl infusions. Overall, changes in RBF were unrelated to changes in PNa or fractional Na or fluid reabsorption but correlated with changes in P(:I (r = -0.91) and fractional Cl-reabsorption (r = 0.94). The intrafemoral arterial infusion of the two Cl-containing solutions did not increase femoral vascular resistance. In conclusion, hyperchloremia produces a progressive renal vasoconstriction and fall in GFR that is independent of the renal nerves, is potentiated by prior salt depletion and is related to tubular Cl-reabsorption. Chloride-induced vasoconstriction appears specific for the renal the adequacy of the extracellular volume (ECV)' is threatened by salt depletion, impaired proximal tubule reabsorption or a high perfusion pressure, renal vasoconstriction restricts the volume of filtrate delivered to the tubules (1-5). A mechanism that can relate glomerular filtration to distal fluid delivery has been identified in micropuncture experiments in which single nephron glomerular filtration rate (SNGFR) has been found to fall during a selective increase in the Na+ or Cl-concentrations or osmolality of early distal tubule fluid (6-8).In previous experiments, we (9) and others (10, 11) showed that intrarenal infusion of hypertonic NaCI solution causes transient vasodilatation followed by sustained vasoconstriction. Schnermann et al. (8) demonstrated that retrograde injection of Cl-containing solutions into the distal tubule regularly elicited a decrease in SNGFR, whereas similar injections of Nacontaining solutions did not. In contrast, in experiments on the isolated kidney, Nizet (12-14) concluded that there was no specific effect of increased Na+ or Cl-concentration on renal vascular resistance but that the GFR varied in direct proportion to tubular fluid reabsorption. To settle these differences between the responses of the isolated kidney...

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Section: Experimental Protocolmentioning

confidence: 99%

mentioning

confidence: 99%

Regulation of Renal Blood Flow by Plasma Chloride

Wilcox¹

1983

J. Clin. Invest.

599

340

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“…Consistent with this view is the fact that the elimination of this control leads to a substantial increase of GFR, provided the systemic blood pressure remains normal (for literature see Schnermann & Briggs, 1985) and, further, that experimental stimulation of this mechanism, for instance by proximally acting diuretics, decreases GFR (Persson & Wright, 1982). Under conditions of chronic volume expansion, this mechanism is completely reset (Dev, Drescher & Schnermann, 1974;Hiiberle & Davis, 1982; and GFR escapes from TGF control. This can be inferred from the similarity of nephron filtration rates (SNGFR) measured either by proximal or distal tubular fluid collection, i.e.…”

Section: Introductionmentioning

confidence: 93%

“…variations of the sodium chloride concentration in the macula densa segment (Hiiberle & Davis, 1982. However, during chronic salt loading GFR and blood flow are not increased (Dev et al 1974;Arendshorst & Finn, 1977;Johnston, Bernard, Perrin, Arbeit, Lieberthal & Levinsky, 1981) as experiments in which the control of the GFR by TGF is acutely eliminated would suggest. Provided that observations obtained on superficial cortical nephrons are representative of the entire nephron population, it must be concluded that chronic volume expansion changes additional determinants of glomerular filtration.…”

Section: Introductionmentioning

confidence: 94%

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The control of glomerular filtration rate and renal blood flow in chronically volume‐expanded rats.

Davis¹,

Häberle²,

Kawata³

1988

The Journal of Physiology

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SUMMARY1. Chronic volume expansion by dietary salt loading practically abolishes tubuloglomerular feed-back (TGF) by means of a humoral inhibitor in tubular fluid. Elimination of the vasoconstrictor influence of feed-back does not, however, increase glomerular filtration rate (GFR) and renal blood flow (RBF), implying that chronic salt loading induces additional preglomerular vasoconstriction. This being so, the feed-back response which, although absent in free-flowing nephrons, can still be elicited by loop of Henle perfusion with Ringer solution, should be essentially normal, except that nephron GFR at any loop perfusion rate should be lower than in controls. Persistance of RBF, GFR and nephron GFR autoregulation would imply that autoregulation is achieved by a preglomerular resistance control system independent of feed-back.2. These hypotheses were tested by clearance and micropuncture experiments in rats chronically fed a diet containing 40 g NaCl (kg food)-'.3. RBF and GFR autoregulation indeed persisted, the former down to 90 mmHg compared with 105 mmHg in controls. In controls, nephron GFR measured distally was autoregulated down to 90 mmHg whereas that measured proximally was autoregulated only above 105 mmHg. In high-salt rats nephron GFR from both sites was autoregulated to 90 mmHg.4. Loop of Henle perfusion with homologous tubular fluid in high-salt rats confirmed attenuation of feed-back. Loop perfusion with Ringer solution yielded a response comparable to that in controls (maximal reduction of nephron GFR to 57 %, compared with 56 % in controls). Absolute nephron GFR at any loop perfusion rate was lower in high-salt rats than in controls.5. These observations confirm the initial hypotheses. Considering feed-back and autoregulation as independent, preglomerular resistance control mechanisms, together with elementary haemodynamic considerations, allows formulation of a renal haemodynamics model whose quantitative predictions regarding characteristics of RBF, GFR and feed-back control are remarkably consistent with the literature.

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Renal Circulation

Knox

Spielman

1983

Comprehensive Physiology

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Resetting of tubulo-glomerular feedback sensitivity by dietary salt intake

Cited by 64 publications

References 31 publications

Regulation of Renal Blood Flow by Plasma Chloride

Regulation of Renal Blood Flow by Plasma Chloride

The control of glomerular filtration rate and renal blood flow in chronically volume‐expanded rats.

Renal Circulation

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