Effect of Acute Changes in Glomerular Filtration Rate on Water and Electrolyte Excretion: Mechanism of Denervation Diuresis

Surtshin, A.; Cb, Mueller; Hl, White

doi:10.1152/ajplegacy.1952.169.1.159

Cited by 34 publications

(17 citation statements)

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“…In 25 minutes. As previously explained, this procedure was designed to produce an increase in cerebral sodium concentration comparable to that achieved in this region by the intravenous administration of 100 ml.…”

Section: Methodsmentioning

confidence: 99%

Renal Excretion of Sodium in Arterial Hypertension

et al. 1959

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Patients with arterial hypertension excrete a sodium load more rapidly than do individuals with normal blood pressure. The relationship of this abnormal sodium excretory response to blood pressure and such extrarenal factors as the central nervous system, dietary salt intake, body fluid volume and sodium content, and the adrenal glands has been studied. On the basis of this and other evidence, it is suggested that the exaggerated natriuresis is the result of a renal tubular defect which occurs after the development of hypertension.IT HAS been recognized since the studies of Farnsworth and Barker' that there is an abnormally high renal excretion of chloride in hypertensive individuals. Most subsequent research has been concerned with sodium rather than chloride. There have been several reports2-7 in which subjects with essential hypertension were observed to excrete an intravenous sodium load more rapidly than individuals with normal blood pressure. The explanation has been offered that this excretory derangement is related to alterations in renal function and that the high salt excretors were those hypertensive subjects whose renal plasma flow was reduced and filtration fraction elevated.8 Others,5' 6 however, have failed to observe such a relationship between increased sodium output and renal hemodynainics. The parallelism of the sodium clearance with both the level of the blood pressure2 4-6 9, 10 and renal vascular resistance6 suggested to The present study was undertaken to characterize further the hypertensive pattern of sodium excretion and the factors contributing to it. Consideration was given to the followinig: (1) the relationship of sodium excretion to blood pressure in subjects with labile, essential, and secondary hypertension; (2) the influence of extrarenal factors, such as the central nervous system, dietary salt intake, body fluid volume and sodium content, and the adrenal glands. MATERIALS AND METHODSThe studies were performed on the following subjects: 16 with essential hypertension of varying severity, 4 with labile hypertension, 4 with secondary hypertension, and 11 with normal blood pressure. In the presentation of the data, the subjects with essential hypertension have been grouped in order of increasing blood pressure as follows: for 2 patients with severe essential hypertension and diminished glomerular filtration there was no evidence of renal functional impairment. Cardiac decompensation was absent in all patients. The degree of retinopathy in the subjects with elevated blood pressure was grade II or less. There was no dietary restriction except when the effect of salt intake was being studied. No patient was receiving antihypertensive drugs.Procedures, except when noted, were carried out at approximately the same time in the morning. Water and food were withheld from the preceding midnight until the completion of the study. The subjects were in the supine position. Whenever possible urines were collected through a soft rubber, nmultiholed, indwelling urethral catheter. In the remai...

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Section: Methodsmentioning

confidence: 99%

Renal Excretion of Sodium in Arterial Hypertension

et al. 1959

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“…It has long been known that renal denervation leads to diuresis and natriuresis in several mammalian species (1)(2)(3)(4)(5)(6). Recent studies suggest that this "denervation diuresis" is mainly the result of an effect of the renal nerves on tubular function (1)(2)(3).…”

Section: Introductionmentioning

confidence: 99%

“…Recent studies suggest that this "denervation diuresis" is mainly the result of an effect of the renal nerves on tubular function (1)(2)(3). There are, however, contradictory results and it has been suggested by some (4,5) that the responses are due to an increased filtered load of sodium, secondary to increases in renal plasma flow (RPF)' and glomerular filtration rate (GFR).…”

Section: Introductionmentioning

confidence: 99%

Effects of acute unilateral renal denervation in the rat.

Bello‐Reuss¹,

Colindres²,

Pastoriza-Munoz³

et al. 1975

J. Clin. Invest.

215

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A B S T R A C T Studies were undertaken to characterize the renal responses to acute unilateral renal denervation and the mechanisms involved in these responses. Denervation was produced in anesthetized nondiuretic rats by application of phenol to the left renal artery. Studies were also performed in sham-denervated nondiuretic rats. Whole kidney and individual nephron studies were performed before and after denervation or sham denervation. Denervation increased urine volume from the left kidney to about twice its control value (P < 0.001) and increased urinary sodium excretion from 332 neq min' to 1,887 neq min' (P <0.001). Glomerular filtration rate (GFR) and renal plasma flow (RPF) remained unchanged in both kidneys after the procedure. The innervated right kidney showed no changes in urine volume or in sodium excretion. After denervation, late proximal ratio of tubular fluid inulin concentration to that of plasma [ (F/P) In] decreased from 2.23 to 1.50 (P < 0.001) while single nephron GFR remained unchanged. Absolute reabsorption decreased from 16.5 to 9.9 nl min' (P <0.001). (F/P) i ratios were also decreased in early distal (from 6.21 to 3.18, P <0.001) and late distal convolutions (from 16.41 to 8.33, P < 0.001) during the experimental period. (F/P) Na ratios remained unchanged in the early distal convolutions, but increased from 0.18 to 0.38 (P < 0.01) in late distal convolutions after denervation. Absolute Na reabsorption after denervation increased in the loop of Henle, distal convolution, and collecting ducts. Any changes in intrarenal hydrostatic pressures

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“…Acute or chronic denervation of the kidney results in a moderate increase in electrolyte and water excretion, often described as a "denervation diuresis" (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12). The mechanism of the natriuresis that is a feature of this phenomenon remains controversial.…”

mentioning

confidence: 99%

“…The mechanism of the natriuresis that is a feature of this phenomenon remains controversial. A number of investigators (1)(2)(3)(4)(5) have suggested that nerves alter sodium excretion indirectly by controlling renal hemodynamics, because in their studies there was a rise in filtered sodium large enough to explain the sodium diuresis. Other workers (6)(7)(8)(9)(10)(11)(12) have concluded that denervation depresses tubular transport of sodium.…”

mentioning

confidence: 99%

The Mechanism of Denervation Natriuresis *

Kamm¹,

Levinsky²

1965

J. Clin. Invest.

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Acute or chronic denervation of the kidney results in a moderate increase in electrolyte and water excretion, often described as a "denervation diuresis" (1-12). The mechanism of the natriuresis that is a feature of this phenomenon remains controversial. A number of investigators (1-5) have suggested that nerves alter sodium excretion indirectly by controlling renal hemodynamics, because in their studies there was a rise in filtered sodium large enough to explain the sodium diuresis. Other workers (6-12) have concluded that denervation depresses tubular transport of sodium. At least two factors probably account for the conflicting conclusions. First, there is the technical problem of accurately measuring the small changes in filtered sodium that occur after section of renal nerves. Second, there are no independent data from which one can determine the effect of an increase in filtered sodium uncomplicated by a change in tubular reabsorptive capacity. Therefore, even if a small increase in filtered sodium after nerve section is reliably demonstrated, it is uncertain how large an increase in sodium excretion can be ascribed solely to this change. Results that demonstrate a simultaneous rise in sodium excretion and filtered sodium after denervation, although suggestive, do not conclusively separate a cause and effect relation from simple association.

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Effect of Acute Changes in Glomerular Filtration Rate on Water and Electrolyte Excretion: Mechanism of Denervation Diuresis

Cited by 34 publications

References 0 publications

Renal Excretion of Sodium in Arterial Hypertension

Renal Excretion of Sodium in Arterial Hypertension

Effects of acute unilateral renal denervation in the rat.

The Mechanism of Denervation Natriuresis *

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