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Research Article Free access | 10.1172/JCI105618
Department of Internal Medicine, Yale University School of Medicine, New Haven, Conn.
Department of Pathology, Yale University School of Medicine, New Haven, Conn.
†Work done during the tenure of a research fellowship supported by training grant T1AM5015 from the U. S. Public Health Service.
‡U. S. Public Health Service Research Career Development Award K3-HE 13683.
§U. S. Public Health Service Research Career Award K6-AM-21578.
Address requests for reprints to D. Franklin H. Epstein, Dept. of Internal Medicine, Yale University School of Medicine, New Haven, Conn.
*Submitted for publication January 16, 1967; accepted April 13, 1967.
Supported by research grants from the U. S. Public Health Service (AM07369 and HE00834) and the American and Connecticut Heart Associations.
Find articles by Hayslett, J. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, Yale University School of Medicine, New Haven, Conn.
Department of Pathology, Yale University School of Medicine, New Haven, Conn.
†Work done during the tenure of a research fellowship supported by training grant T1AM5015 from the U. S. Public Health Service.
‡U. S. Public Health Service Research Career Development Award K3-HE 13683.
§U. S. Public Health Service Research Career Award K6-AM-21578.
Address requests for reprints to D. Franklin H. Epstein, Dept. of Internal Medicine, Yale University School of Medicine, New Haven, Conn.
*Submitted for publication January 16, 1967; accepted April 13, 1967.
Supported by research grants from the U. S. Public Health Service (AM07369 and HE00834) and the American and Connecticut Heart Associations.
Find articles by Kashgarian, M. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, Yale University School of Medicine, New Haven, Conn.
Department of Pathology, Yale University School of Medicine, New Haven, Conn.
†Work done during the tenure of a research fellowship supported by training grant T1AM5015 from the U. S. Public Health Service.
‡U. S. Public Health Service Research Career Development Award K3-HE 13683.
§U. S. Public Health Service Research Career Award K6-AM-21578.
Address requests for reprints to D. Franklin H. Epstein, Dept. of Internal Medicine, Yale University School of Medicine, New Haven, Conn.
*Submitted for publication January 16, 1967; accepted April 13, 1967.
Supported by research grants from the U. S. Public Health Service (AM07369 and HE00834) and the American and Connecticut Heart Associations.
Find articles by Epstein, F. in: JCI | PubMed | Google Scholar
Published July 1, 1967 - More info
Acute infusions of isotonic saline in the rat cause an increase in glomerular filtration rate and in the excretion of salt and water. The kidney swells, due to expansion of tubular and interstitial volume. Despite the increase in tubular diameter, transit time through the proximal tubules and loops of Henle is decreased, presumably owing to a greatly accelerated rate of tubular flow. Proximal tubular reabsorption, measured in blocked tubules, is inhibited in a way that cannot be ascribed to changes in tubular diameter. The prolongation of proximal reabsorptive half-time is not affected by the administration of aldosterone. It occurs equally in rats chronically loaded with or deprived of salt, and it is therefore not likely that it is influenced by the renal content of renin. In contrast, reabsorption from the distal convoluted tubule is enhanced by saline infusion. This change is observed in segments of tubules blocked with oil and isolated from their glomeruli and thus appears to occur independently of changes in glomerular filtration or tubular flow.
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