Mar. 28, 2011 A new finding shows how the million working units in the kidney regulate salt handling. This identifies a new possible therapeutic target for treating high blood pressure. The kidney is made up of roughly 1 million working units called nephrons. These basic structural units remove waste products from the blood, recycle some substances to be reused and eliminate what is left as urine. The end segment of nephrons, called the distal nephron, helps set blood pressure by controlling the amount of sodium in our blood.
Scientists at The University of Texas Health Science Center San Antonio have reported how this essential function of the distal nephron is regulated. They demonstrated that sodium handling by the distal nephron is under the control of a local regulatory system.
Loss or dysfunction of this system leads to hypertension resulting from improper salt retention by the kidneys, the scientists found in mouse studies.
"These studies provide the first unequivocal evidence of a blood pressure control system in the distal nephron of the kidney," said senior author James Stockand, Ph.D., professor of physiology at the Health Science Center. "It turns out control of sodium re-absorption by this system is as important to normal blood pressure regulation as is a better-understood system, called the renin-angiotensin-aldosterone system, which works outside the kidney."
Many medications that treat high blood pressure target salt handling in the kidney. "Our work identifies a possible new therapeutic target," Dr. Stockand said.
The research was funded by the U.S. National Institutes of Health and American Heart Association and included colleagues at the University of Southern California. The findings are in the Jan. 14 issue of the Journal of Biological Chemistry.
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The above story is based on materials provided by University of Texas Health Science Center at San Antonio, via EurekAlert!, a service of AAAS.
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- E. Mironova, J. Peti-Peterdi, V. Bugaj, J. D. Stockand. Diminished Paracrine Regulation of the Epithelial Na Channel by Purinergic Signaling in Mice Lacking Connexin 30. Journal of Biological Chemistry, 2010; 286 (2): 1054 DOI: 10.1074/jbc.M110.176552
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