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Their Effect on the Refractory Phase

ROBERT H. SELLER, MD; CHARLES D. SWARTZ, MD; OSWALDO RAMIREZ-MUXO, MD; ALBERT H. BREST, MD; JOHN H. MOYER, MD

Arch Intern Med. 1964;113(3):350-355.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Since 1955, when the clinical picture of aldosteronism was first described, the substance aldosterone has aroused the interest of the physiologist, pharmacologist, renologist, and clinician.¹ Conditions associated with increased aldosterone activity can be divided into two broad groups (primary and secondary) depending on whether their cause is intrinsic or extrinsic to the adrenal cortex.² Adrenal tumor, adrenal hyperplasia, and "congenital" hyperaldosteronism are examples of the primary forms. Conditions in which aldosteronism is secondary to another disease state include malignant hypertension,³ renovascular hypertension,³ refractory heart failure,⁴ nephrotic syndrome,⁵ and cirrhosis with ascites.⁶

Clinical and experimental observations have demonstrated that after initial fluid depletion induced by the administration of a diuretic agent, an antidiuretic phase frequently ensues.⁷ The mechanisms underlying the loss of responsiveness and the antidiuretic phase are not precisely defined, but aldosteronism is probably an important factor. Other studies have shown that salt restriction in both normal and edematous patients . . . [Full Text PDF of this Article]

Author Affiliations
PHILADELPHIA

Associate in Medicine (Dr. Seller); Research Fellow of the US Public Health Service (contract No. HF-14,455) (Dr. Swartz); Research Fellow (Dr. Ramirez-Muxo); Head of Hypertension-Renal Unit (Dr. Brest); Chairman of Department of Medicine (Dr. Moyer).

From the Hypertension-Renal Unit of the Department of Medicine, Hahnemann Medical College and Hospital.

Footnotes
Received for publication May 29, 1963; accepted Sept 12.

This paper was presented in part at the 35th Scientific Session of the American Heart Association, October, 1962.

The study was supported by grants from the National Institute of Arthritis and Metabolism (No. AM-04908), Smith, Kline and French Laboratories, and G. D. Searle & Co.

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