Stages of Salt Exchange in Essential Hypertension

Green, D. M.; Johnson, A. D.; Bridges, W. C.; Lehmann, J. H.

doi:10.1161/01.cir.9.3.416

Cited by 21 publications

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“…2 We subsequently showed that the tendency of hypertensive patients toward increased sodium excretion could be elicited not only by hypertonic saline loads, but by mannitol and isotonic saline loads as well. 3 A lower, but still significant, correlation between the blood pressure of patients and their urinary sodium output was also demonstrated under basal conditions.' In comparable animal studies we had found that the basal output of sodium was directly proportional to its antecedent intake in the diet.…”

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confidence: 91%

Sodium Output—Blood Pressure Relationships and Their Modification by Treatment

Green

Ellis

1954

Circulation

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confidence: 91%

Sodium Output—Blood Pressure Relationships and Their Modification by Treatment

Green

Ellis

1954

Circulation

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“…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 This work is supported by the Johln A. Hartford Foundation and the Eda K. Loeb Fund.…”

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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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“…Whereas three of the subjects manifested an exaggerated natriuresis, the remaining two manifested responses not differing from that of normal subjects. Green et al 7 studied renal sodium and water handling in 26 nonhypertensive controls and 53 patients with hypertension and observed that the hypertensive patients could be divided into a "normal sodium-excreter" group and a "high sodium-excreter" group (« = 18). During the saline infusion test, the high sodium-excreter group excreted sodium at a mean rate of 535 ± 182 /xEq/min, a level approximately threefold greater than that of the normal sodium-excreter hypertensive subjects.…”

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Spectrum of deranged sodium homeostasis in essential hypertension.

Epstein¹,

Loutzenhiser²,

Levinson³

1986

Hypertension

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SUMMARY Essential hypertension is thought to produce a uniform exaggerated natriuresis and diuresis. Because validation of this formulation in humans is incomplete, the natriuretic and diuretic responses to acute volume expansion were characterized by using water immersion to the neck. This method provides a volume stimulus identical to that induced by 2 L of saline without plasma compositional change. Twenty-seven subjects with essential hypertension were studied on three occasions in the seated posture while in balance on a 10 mEq Na, 100 mEq K diet: during the seated control study, during 4 hours of head-out immersion, and during saline infusion (2 L/2 hours). Four subjects had exaggerated urinary Na excretion in response to neck immersion (Group 3), and 16 had a normal response (Group 2) indistinguishable from that of 15 previously studied normal subjects. The remaining seven subjects (Group 1) had blunted or absent natriuretic responses compared with that in normal subjects (p < 0.005). Similar results were obtained with saline administration; cumulative Na excretion in Group 1 was markedly less than that in Group 2 and the normal subjects. The heterogeneity in Na excretion indicates that an exaggerated natriuresis is not a uniform concomitant of essential hypertension. The significant inverse correlation between basal plasma aldosterone level and peak urinary as well as cumulative Na excretion suggests that plasma aldosterone constitutes a determinant of the differing natriuretic responses. In contrast to findings with urinary Na excretion, the diuretic responses of Groups 1 and 2 were identical. The striking dissociation between renal Na and water handling underscores the specificity of the derangement in renal Na handling.

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Stages of Salt Exchange in Essential Hypertension

Abstract: The relation of sodium to hypertension remains one of the most fascinating problems in medicine.The results accumulated over a five-year period of study of this relationship are presented in the paper which follows. In these investigations the appetite for salt and the output of

Cited by 21 publications

References 3 publications

Sodium Output—Blood Pressure Relationships and Their Modification by Treatment

Sodium Output—Blood Pressure Relationships and Their Modification by Treatment

Renal Excretion of Sodium in Arterial Hypertension

Spectrum of deranged sodium homeostasis in essential hypertension.

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