Effect of an Intravenous Sodium Chloride Load on Renal Hemodynamics and Electrolyte Excretion in Essential Hypertension

Cottier, P; Weller, John M.; Hoobler, Sibley W.

doi:10.1161/01.cir.17.4.750

Cited by 94 publications

(24 citation statements)

References 15 publications

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“…Further, it was found in the present study that the excretion of Na became greater with an advance of hypertension as far as the renal function was normal. It seems, as indi cated by Cottier,13) that the " high salt-excretor " corresponds with the stage where the renal function is not impaired and the " normal salt excretor " with the stage where the renal function is damaged.…”

Section: Effect On Minute Electrolytes Excretionmentioning

confidence: 94%

Effect of Salt Loading on Renal Hemodynamics and Electrolytes Excretion in Essential Hypertension and in Chronic Glomerulonephritis

Sasamori

1960

Tohoku J. Exp. Med.

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In 1905, Ambard and Beaujard1) found that the administration of NaCl to the patients with hypertension produced a further increase in blood pressure and the restriction of salt resulted in a fall of blood pressure in these patients. Since then, many studies have been attempted to in vestigate the participation of sodium chloride in the occurrence of hyper tension. Dahl2) investigated the daily salt intake in 1300 subjects and found the high incidence of hypertension in the subjects who took a larger amount of salt. Itahara and others") have pointed out, that in the north-eastern district, especially in Akita prefecture, of Japan, where the incidence of hypertension and apoplectic attack is significantly high, compared with that in the other districts, the people use to take up an excess of salt in the daily diet. They are at present making effort to improve the diet, restricting the salt intake, and it is now said that the occurrence of those diseases is decreasing, though slightly, year by year. Sapierstein and his collaborators') succeeded in producing a permanent hypertension in rats by administrating hypertonic saline solution every day for a long time. It was reported by Laramore4) and Eichelberger5) that the salt content of the muscles was higher in animals with experimental hypertension.

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Section: Effect On Minute Electrolytes Excretionmentioning

confidence: 94%

Effect of Salt Loading on Renal Hemodynamics and Electrolytes Excretion in Essential Hypertension and in Chronic Glomerulonephritis

Sasamori

1960

Tohoku J. Exp. Med.

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“…However, this pattern has been described in subjects with established hypertension and in response to an acute saline load producing rapid extracellular volume expansion. 33 " 35 More recent investigations have demonstrated a heterogeneity in sodium excretion rates after saline loads in hypertensive patients. 36 Rydstedt et al 37 studied sodium excretion rates after saline infusion in hypertensive individuals grouped by before sodiumloading renin levels.…”

Section: -29mentioning

confidence: 99%

Effect of chronic sodium loading on cardiovascular response in young blacks and whites.

1990

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The effect of long-term oral sodium loading on blood pressure and on stress-induced cardiovascular response was studied in normotensive and marginally hypertensive young adults. The 121 subjects, 18-23 years old, included 38 whites and 83 blacks. Blood pressure and heart rate response to the stress of mental arithmetic was measured before and after 14 days of sodium load, which consisted of 10 g NaCl/day added to the usual diet. A sodium-sensitive response to sodium load occurred in 18.4% of whites and 37.3% of blacks. Sodium-insensitive subjects had a higher rate of sodium excretion (p<0.001). Sodium-sensitive hypertensive subjects had a significantly greater weight gain (p<0.001). A significant correlation between blood pressure change and sodium excretion (r=-0.28, p<0.01) occurred in the sodiumsensitive group. The high sodium intake did not augment the blood pressure or heart rate response to the ^-adrenergic-mediated stimulus of mental arithmetic in the population when grouped by blood pressure, race, or sodium sensitivity. These results suggest that blood pressure increase in response to sodium load, particularly in blacks, is related to functional changes in peripheral vascular resistance. (Hypertension 1990;15:36-43) T he prevalence of hypertension is greater in black adults than in whites.

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“…Numerous investigators have demonstrated that acute volume expansion in patients with hypertension results in a more prompt rise in sodium excretion than is seen in the normotensive subject (1)(2)(3). This phenomenon, which has been referred to as an "exaggerated natriuresis," has been attributed both to decreased tubular sodium reabsorption (2,3) and to increased glomerular filtration rate (GFR) (2), but the intrarenal mechanisms have not been precisely defined.…”

Section: Introductionmentioning

confidence: 99%

Mechanism of exaggerated natriuresis in hypertensive man: impaired sodium transport in the loop of henle

Buckalew¹,

Puschett²,

Kintzel³

et al. 1969

J. Clin. Invest.

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A B S T R A C T To evaluate the effects of saline loading on distal sodium reabsorption in hypertensive man, studies were performed during both water deprivation and water diuresis in eight hypertensive subjects, and the results were compared to data obtained from similar studies in normal subjects. All hypertensive patients exhibited an enhanced excretion of filtered sodium (Ca/CIn) at any level of distal delivery of sodium compared to normal controls. Free water reabsorption (TCH2o) during hypertonic saline loading was quantitatively abnormal in the hypertensives at high levels of osmolar clearance (Co.m), and also the curve of TCHIo vs. Co.m leveled off above a Co.m of 18 ml/min per 1.73 m' in the hypertensive group in contrast to the normal controls in whom TCH,0o showed no evidence of achieving an upper limit. Sodium depletion exaggerated the abnormality in T'Ho in hypertensives, and resulted in a positive free water clearance (CH2o) during hydropenia.During hypotonic saline loading in water diuresis, changes in free water clearance per 100 ml of glomerular filtrate (CIo0/CI.) were less at any given increment in urine flow per 100 ml of glomerular filtrate (V/CG.) in the hypertensives compared to normal controls (P < 0.001). This abnormality in CH2o/CI. in the hypertensives in conjunction with the defect in T'H2o observed during hydropenia indicates that sodium reabsorption in the loop of Henle was abnormal at any given rate of distal delivery of sodium in hypertension. Furthermore, these abnormalities in TCH2o and CH20 coincided temporally with the development of the exaggerated natriuresis. Although the distal defect in sodium transport, in large part, accounted for the augmented natriuresis in hyperThis work was presented in part at the 1st Annual Meeting of the

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Effect of an Intravenous Sodium Chloride Load on Renal Hemodynamics and Electrolyte Excretion in Essential Hypertension

Cited by 94 publications

References 15 publications

Effect of Salt Loading on Renal Hemodynamics and Electrolytes Excretion in Essential Hypertension and in Chronic Glomerulonephritis

Effect of Salt Loading on Renal Hemodynamics and Electrolytes Excretion in Essential Hypertension and in Chronic Glomerulonephritis

Effect of chronic sodium loading on cardiovascular response in young blacks and whites.

Mechanism of exaggerated natriuresis in hypertensive man: impaired sodium transport in the loop of henle

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