Renal Excretion of Sodium in Arterial Hypertension

Abstract

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...

The Response to the Administration of an Isotonic Sodium Chloride-Lactate Solution in Patients With Essential Hypertension

“…The possibility exists that the renal tubular cell itself is abnormal or that a normal tubular cell is responding normally to abnormal influences or to stimuli that are abnormally mediated. While a specific tubular "defect" cannot be excluded, there is little evidence in support of this concept (7). Among the variety of known and unknown extrarenal factors that might influence renal tubular handling of sodium in the hypertensive patient are hormonal factors (e.g., adrenocortical and adrenomedullary), neurogenic factors and intrarenal circulatory phenomena (8).…”

“…(Submitted for publication December 21, 1959; accepted January 8, 1960) Many studies indicate that patients with essential hypertension have a greater natriuretic response to rapidly administered sodium chloride solutions than have normotensive individuals (1)(2)(3)(4)(5)(6)(7). However, in most instances other factors known to influence the rate of sodium excretion in the normal subject such as diet, posture, and time of day have not been rigidly controlled (8,9).…”

Augmented Natriuretic Response to Acute Sodium Infusion after Blood Pressure Elevation with Metaraminol in Normotensive Subjects *

“…This phenomenon has been repeatedly reported in patients with essential hypertension (1)(2)(3)(4)(5). Patients with hypertension caused by chronic glomerulonephritis (9, 10), Cushing's syndrome (4, 6, 7), pheochromocytoma (4), primary aldosteronism (8,11), and unilateral renal disease (10) have also been reported to have an exaggerated natriuretic response to acute salt loading, suggesting that elevated blood pressure could be a common denominator in this phenomenon.…”

“…That patients with essential hypertension have an exaggerated natriuretic response to the rapid intravenous administration of sodium is well established (1)(2)(3)(4)(5). Other hypertensive states have also been reported to exhibit an exaggerated natriuretic response to acute salt loading (4,(6)(7)(8)(9)(10)(11).…”

“…Other hypertensive states have also been reported to exhibit an exaggerated natriuretic response to acute salt loading (4,(6)(7)(8)(9)(10)(11). Although the mechanisms responsible for this phenomenon remain unknown (5), one of the possibilities is that the elevation of the blood pressure per se may cause the enhanced natriuresis (10).…”