Vardaman M. Buckalew, Jules B. Puschett, James E. Kintzel, Martin Goldberg
J Clin Invest.
1969;
48(6):1007–1016
doi:10.1172/JCI106057
This article Copyright © 1969, The American Society for Clinical Investigation
Abstract
|
Full text
|
PDF
T
o 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 (CNa/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 (COsm), and also the curve of TcH2O vs. COsm leveled off above a COsm of 18 ml/min per 1.73 m2 in the hypertensive group in contrast to the normal controls in whom TcH2O showed no evidence of achieving an upper limit. Sodium depletion exaggerated the abnormality in TcH2O 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 (CH2O/CIn) were less at any given increment in urine flow per 100 ml of glomerular filtrate (V/CIn) in the hypertensives compared to normal controls (P < 0.001). This abnormality in CH2O/CIn in the hypertensives in conjunction with the defect in TcH2O 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 CH2O 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 hypertension, evidence was present also for enhanced rejection of sodium in the proximal tubule during saline loading in the hypertensives.Additional studies utilizing acetazolamide which increases distal delivery of sodium without extracellular fluid volume expansion showed only minimal abnormalities in CH2O in the hypertensive group, indicating that the defect in sodium transport in the loop of Henle in hypertensives is mainly an abnormal response to extracellular fluid expansion rather than an intrinsic defect in the loop to handle increased tubular loads of sodium. It is possible that the abnormality in sodium reabsorption in the loop of Henle is due to the transmission of the abnormally elevated blood pressure of the hypertensives to the medullary vasa recta during saline loading.
This file is in Adobe Acrobat (PDF) format.
If you have not installed and configured the Adobe Acrobat Reader on your system.
Having trouble reading a PDF?
PDFs are designed to be printed out and read, but if you prefer to read them online, you may find it easier if you increase the view size to 125%.
Having trouble saving a PDF?
Many versions of the free Acrobat Reader do not
allow Save. You must instead save the PDF from the JCI Online page you downloaded it from. PC users:
Right-click on the Download link and choose the option that says something like "Save Link As...".
Mac users should hold the mouse button down on the link to get these same options.
Having trouble printing a PDF?
- Try printing one page at a time or to a newer printer.
- Try saving the file to disk before printing rather than opening it "on the fly." This requires that you
configure your browser to "Save" rather than "Launch Application" for the file type "application/pdf", and can
usually be done in the "Helper Applications" options.
- Make sure you are using the latest version of Adobe's Acrobat Reader.