Up to one-third of American adults suffer from some form of high blood pressure (hypertension), according to estimates by the U. S. Centers for Disease Control (CDC). The costs associated with the condition are staggering, estimated to have reached more than $76 billion last year alone.
Often, hypertension is linked to fluid retention and excess salt. Scientists attending an international symposium sponsored by the American Physiological Society this week, in Pacific Grove, California, learned new information about the links among kidney disease, fluid and salt retention, and hypertension.
The kidneys filter 150 to 200 quarts of blood daily, and play a central role in blood pressure regulation due to this filtration activity. Individual filtration units, called nephrons, consist of a filtration apparatus called the glomerulus, which is attached to a tubule. Filtered blood enters the tubules, where various substances are either added or removed.
When things are working properly, excess water and salt are removed and excreted as urine. But in patients with damaged kidneys - a common condition called nephrotic syndrome - the kidneys may fail to remove these excess substances, returning them to the bloodstream. Fluid retention results, and this may eventually cause hypertension or edema (swelling due to fluid retention).
New research described at the symposium explained some of the precise mechanisms by which this process occurs. For instance, Thomas R. Kleyman, Professor of Medicine and of Cell biology and Physiology at the University of Pittsburgh School of Medicine, and Ole Skott, Professor of Physiology and Pharmacology and Dean at the University of Southern Denmark in Odense, independently discovered that damaged filtration barriers allow a protein called plasminogen to enter the tubules, where it is converted into a second substance, plasmin.
Plasmin helps activate the epithelial sodium channel (ENaC) on cells in the nephron, the scientists reported. ENaC enables the absorption of filtered sodium from tubules; when it becomes overactive, excessive absorption of filtered sodium causes sodium and water retention.
This new insight into the relationships among kidney damage, salt retention and high blood pressure offers a potential new avenue for treatment of the disease process. "...If plasmin activates ENaC, it suggests that targeting ENaC in the kidneys with ENaC inhibitors may be a treatment option," said Dr. Kleyman.
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