Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1969;39:685-692

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by ADLIN, E. V.
Right arrow Articles by MARKS, A. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by ADLIN, E. V.
Right arrow Articles by MARKS, A. D.

(Circulation. 1969;39:685.)
© 1969 American Heart Association, Inc.


Salivary Sodium-Potassium Ratio and Plasma Renin Activity in Hypertension

E. VICTOR ADLIN M.D.1; BERTRAM J. CHANNICK M.D.1; ALLAN D. MARKS M.D.1

1 From the Section of Endocrinology, Department of Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania.

The cause of the suppression of plasma renin activity (PRA) in many patients with essential hypertension and normal aldosterone excretion is unknown. Since mineralocorticoid excess can lower PRA, we attempted to evaluate the activity of salt-retaining hormones in these patients by measuring the salivary Na/K ratio. The median Na/K ratio in 20 hypertensive patients with suppressed PRA and normal or low aldosterone excretion was 0.71. This was significantly lower than the median of 1.38 in 29 normal subjects and the median of 1.05 in 15 hypertensive patients with normal PRA.

Excess dietary intake of salt is a possible cause of PRA suppression in these patients, but our findings indicate that high rather than low Na/K ratios would be expected if this were present. On the other hand, both the salivary electrolyte changes and the suppression of PRA are consistent with the hypothesis that mineralocorticoid excess is present in these patients, despite the failure to demonstrate elevated excretion of aldosterone.


Key Words: Aldosterone • Urinary sodium and potassium • Mineralocorticoid excess • Plasma potassium • Adrenal adenoma • Excess dietary salt




This article has been cited by other articles:


Home page
Arch Intern MedHome page
E. V. Adlin, A. D. Marks, and B. J. Channick
Racial Difference in Salivary Sodium-Potassium Ratio in Low Renin Essential Hypertension
Arch Intern Med, April 1, 1982; 142(4): 703 - 706.
[Abstract] [PDF]


Home page
Arch Intern MedHome page
S. C. Gulati, B. J. Channick, E. V. Adlin, C. M. Biddle, and A. D. Marks
Low-Renin Hypertension: Occurrence in Vascular Complications
Arch Intern Med, February 1, 1975; 135(2): 260 - 263.
[Abstract] [PDF]


Home page
JAMAHome page
J. G. Douglas, J. W. Hollifield, and G. W. Liddle
Treatment of Low-Renin Essential Hypertension: Comparison of Spironolactone and a Hydrochlorothiazide-Triamterene Combination
JAMA, February 4, 1974; 227(5): 518 - 521.
[Abstract] [PDF]


Home page
Arch Intern MedHome page
E. V. Adlin, A. D. Marks, and B. J. Channick
Spironolactone and Hydrochlorothiazide in Essential Hypertension: Blood Pressure Response and Plasma Renin Activity
Arch Intern Med, December 1, 1972; 130(6): 855 - 858.
[Abstract] [PDF]


Home page
Arch Intern MedHome page
S. Wotman, L. Baer, I. D. Mandel, and J. H. Laragh
Submaxillary Potassium Concentration in True and Pseudoprimary Aldosteronism
Arch Intern Med, August 1, 1970; 126(2): 248 - 251.
[Abstract] [PDF]