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Research Article Free access | 10.1172/JCI105645
Department of Medicine, Harvard Medical School, Boston, Massachusetts
Department of Medicine, Beth Israel Hospital, Boston, Massachusetts
‡Recipient of U. S. Public Health Service Career Development Award 7-K3-HE-12, 113-03.
§Student at Harvard Medical School, recipient of summer fellowship 5T5GM 1651-05 from U. S. Public Health Service.
ǁRecipient of U. S. Public Health Service Career Development Award 1-K3-HE-31,106.
Address requests for reprints to Dr. Philip R. Steinmetz, Beth Israel Hospital, 330 Brookline Avenue, Boston, Mass. 02215.
*Received for publication 8 February 1967 and in revised form 6 June 1967.
Supported by grants from the American Heart Association, the William F. Milton Fund of Harvard University, the John A. Hartford Foundation, and a General Research Support Grant, 5S01 FR 05479-04, from the U. S. Public Health Service.
Presented in part before the annual meeting of the American Society for Clinical Investigation, 1 May 1966, Atlantic City, N. J. (1).
Find articles by Steinmetz, P. in: JCI | PubMed | Google Scholar
Department of Medicine, Harvard Medical School, Boston, Massachusetts
Department of Medicine, Beth Israel Hospital, Boston, Massachusetts
‡Recipient of U. S. Public Health Service Career Development Award 7-K3-HE-12, 113-03.
§Student at Harvard Medical School, recipient of summer fellowship 5T5GM 1651-05 from U. S. Public Health Service.
ǁRecipient of U. S. Public Health Service Career Development Award 1-K3-HE-31,106.
Address requests for reprints to Dr. Philip R. Steinmetz, Beth Israel Hospital, 330 Brookline Avenue, Boston, Mass. 02215.
*Received for publication 8 February 1967 and in revised form 6 June 1967.
Supported by grants from the American Heart Association, the William F. Milton Fund of Harvard University, the John A. Hartford Foundation, and a General Research Support Grant, 5S01 FR 05479-04, from the U. S. Public Health Service.
Presented in part before the annual meeting of the American Society for Clinical Investigation, 1 May 1966, Atlantic City, N. J. (1).
Find articles by Omachi, R. in: JCI | PubMed | Google Scholar
Department of Medicine, Harvard Medical School, Boston, Massachusetts
Department of Medicine, Beth Israel Hospital, Boston, Massachusetts
‡Recipient of U. S. Public Health Service Career Development Award 7-K3-HE-12, 113-03.
§Student at Harvard Medical School, recipient of summer fellowship 5T5GM 1651-05 from U. S. Public Health Service.
ǁRecipient of U. S. Public Health Service Career Development Award 1-K3-HE-31,106.
Address requests for reprints to Dr. Philip R. Steinmetz, Beth Israel Hospital, 330 Brookline Avenue, Boston, Mass. 02215.
*Received for publication 8 February 1967 and in revised form 6 June 1967.
Supported by grants from the American Heart Association, the William F. Milton Fund of Harvard University, the John A. Hartford Foundation, and a General Research Support Grant, 5S01 FR 05479-04, from the U. S. Public Health Service.
Presented in part before the annual meeting of the American Society for Clinical Investigation, 1 May 1966, Atlantic City, N. J. (1).
Find articles by Frazier, H. in: JCI | PubMed | Google Scholar
Published October 1, 1967 - More info
The relationship between hydrogen ion secretion and the transport of other electrloytes was examined in the isolated urinary bladder of the water turtle. Symmetrical solutions which were free from exogenous carbon dioxide and bicarbonate bathed the two surfaces of the preparation, and the spontaneous electrical potential of the bladder was nullified by a voltage clamp. Active transport of sodium from mucosal to serosal medium was confirmed by simultaneous bidirectional flux measurements and found to be slightly, but not significantly, greater than the short-circuit current. In the absence of sodium in the bathing solutions, the normal potential difference across the bladder reversed and the current required to nullify this reversed potential difference had the same magnitude as the simultaneously measured rate of hydrogen ion secretion. The results indicate that, under these experimental conditions, the bladder transports sodium and hydrogen ion actively, but that chloride movement does not contribute to the short-circuit current.
The rate of secretion of hydrogen ion was not affected by replacement of the sodium in the bathing media by cesium, or by inhibition of sodium transport by dinitrophenol. Acidification continued when chloride in the solutions was replaced by sulfate, or when potassium or calcium was removed from the solution bathing the mucosal surface.
Secretion of hydrogen ion by the turtle bladder is not dependent on the simultaneous transport of other electrolytes across the bladder.