Proximal tubular function and salt sensitivity

Burnier, Michel; Bochud, Murielle; Maillard, Marc

doi:10.1007/s11906-006-0035-6

Cited by 27 publications

(32 citation statements)

References 69 publications

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“…We have reported previously that FE Li remains inappropriately low in some hypertensive patients, reflecting an enhanced proximal sodium reabsorption and salt sensitivity. 7 A third possible factor is the smaller decrease in sodium excretion under the LS diet in the hypertensive participants. Although the same dietary regimen was applied to normotensive and hypertensive subjects, the compliance of the latter appears to be less than that of the former.…”

Section: Pruijm Et Al Salt Intake and Renal Oxygenationmentioning

confidence: 99%

“…[1][2][3][4] Patients with essential and secondary forms of hypertension are often characterized by increased sodium retention either in the proximal or in the distal nephron segments. [5][6][7] Experimentally, the renal handling of sodium is a process known to have an important impact on renal tissue oxygen consumption. 8 Indeed, the tubular sodium reabsorption requires active transport systems that are energy consuming.…”

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confidence: 99%

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Effect of Sodium Loading/Depletion on Renal Oxygenation in Young Normotensive and Hypertensive Men

et al. 2010

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Abstract-The goal of this study was to investigate the effect of sodium intake on renal tissue oxygenation in humans. To this purpose, we measured renal hemodynamics, renal sodium handling, and renal oxygenation in normotensive (NT) and hypertensive (HT) subjects after 1 week of a high-sodium and 1 week of a low-sodium diet. Renal oxygenation was measured using blood oxygen level-dependent magnetic resonance. Tissue oxygenation was determined by the measurement of R2* maps on 4 coronal slices covering both kidneys. The mean R2* values in the medulla and cortex were calculated, with a low R2* indicating a high tissue oxygenation. Ten male NT (mean age: 26.5Ϯ7.4 years) and 8 matched HT subjects (mean age: 28.8Ϯ5.7 years) were studied. Cortical R2* was not different under the 2 conditions of salt intake. Medullary R2* was significantly lower under low sodium than high sodium in both NT and HT subjects (28.1Ϯ0.8 versus 31.3Ϯ0.6 s Ϫ1; PϽ0.05 in NT; and 27.9Ϯ1.5 versus 30.3Ϯ0.8 s Ϫ1 ; PϽ0.05, in HT), indicating higher medullary oxygenation under low-sodium conditions. In NT subjects, medullary oxygenation was positively correlated with proximal reabsorption of sodium and negatively with absolute distal sodium reabsorption, but not with renal plasma flow. In HT subjects, medullary oxygenation correlated with the 24-hour sodium excretion but not with proximal or with the distal handling of sodium. These data demonstrate that dietary sodium intake influences renal tissue oxygenation, low sodium intake leading to an increased renal medullary oxygenation both in normotensive and young hypertensive subjects. (Hypertension. 2010;55:1116-1122.)

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Section: Pruijm Et Al Salt Intake and Renal Oxygenationmentioning

confidence: 99%

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confidence: 99%

Effect of Sodium Loading/Depletion on Renal Oxygenation in Young Normotensive and Hypertensive Men

et al. 2010

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“…Burnier et al, 57 using the endogenous renal lithium clearance (Cl Li ) method, a well-validated measure of total proximal tubular sodium reabsorption, found that SS subjects do not suppress proximal sodium reabsorption as effectively as SR ones in response to sodium loading. Cl Li measurements do not permit distinction between the several mechanisms mediating proximal tubular sodium reabsorption, but the finding is consistent with the renal hemodynamic studies reviewed above: the increase in filtration fraction observed in SS hypertensive subjects should increase peritubular oncotic pressure and promote sodium reabsorption in the proximal tubule.…”

Section: Segmental Renal Tubular Sodium Transportmentioning

confidence: 99%

Nocturnal Sodium Excretion, Blood Pressure Dipping, and Sodium Sensitivity

2006

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M ore than 30 years ago, Guyton 1 described pressurenatriuresis: increasing arterial blood pressure promotes sodium excretion, decreasing blood volume and lowering blood pressure, whereas when blood pressure falls, sodium excretion decreases, and blood volume and blood pressure increase. 1,2 The linchpin of the model of Guyton et al 3 is the concept of feedback gain. Gain is the degree to which a feedback system can correct a perturbation, that is, the amount of correction of a deviation divided by the residual degree of deviation. When a control system corrects a perturbation minimally, its feedback gain is near 0. When it corrects it completely, its gain is infinite. As emphasized by Guyton et al,3 in integrated systems with infinite and finite gain components, the infinite gain function ultimately dominates. There are myriad blood pressure control systems, for example, arterial baroreceptors and chemoreceptors, the central nervous system ischemic response, the renin-angiotensin system, and capillary fluid shift, but all are ultimately trumped by pressure-natriuresis. In the experiments by Guyton et al, 3 pressure-natriuresis had near infinite gain over a wide range of urinary sodium excretion, such that the set point of blood pressure regulation was not affected by sodium intake over a period of several days or a few weeks.This pressure-natriuresis model describes a steady-state relationship. At short time intervals, blood pressure and sodium excretion may not be closely linked, but the body will always eventually bring the system back into balance. In this review, we wish to draw attention to differences in the relationship of blood pressure to sodium excretion during day and night and to how nighttime pressure-natriuresis and sodium sensitivity of blood pressure interact. We will suggest that these features of pressure-natriuresis have implications both for the clinical management of hypertension and research into the genetic underpinnings of the disease. Diurnal Rhythm of Sodium Excretion in Normotensive and Hypertensive SubjectsIn healthy people, sodium excretion reaches a maximum during the day and a minimum at night during sleep, and it has long been thought that blood pressure is the primary determinant of nighttime sodium excretion. 4 -7 Centonza et al 8 performed ambulatory blood pressure monitoring over a 26-hour period in normotensive subjects for whom sodium intake was fixed at a moderate amount (170 mmol/day). All of the subjects demonstrated a nocturnal dip in blood pressure with a concomitant dip in sodium excretion. Moreover, there were significant positive correlations between blood pressure and sodium excretion during the night and over 24 hours, as well as during periods of quiet supine wakefulness and postprandial sitting. No similar relationship was apparent when subjects carried out daily activities in the standing position. The authors concluded that the pressure-natriuresis relationship is blunted during upright posture, possibly because of the activation of neurohumoral systems. 8 St...

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“…9 In these black subjects, dietary sodium intake was positively associated with systolic blood pressure in subjects with low FE Li but not in those with high FE Li . The mean urinary sodium excretion per day was ≈50 mmol in these black subjects 9 and 163 mmol in our study subjects. The relationship between blood pressure and sodium renal handling might differ from low to high dietary sodium intake.…”

Section: )mentioning

confidence: 77%

“…Among the complex mechanisms, renal sodium handling must play a major role in the determination of this interindividual variability. 9,10 We hypothesize that sodium dietary intake and renal handling interact to influence blood pressure and believe that illustration of this relationship would be clinically relevant for the prevention and management of hypertension by sodium restriction.…”

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confidence: 99%