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(Hypertension. 1999;33:517-523.)
© 1999 American Heart Association, Inc.

Scientific Contributions

Handling ²²NaCl by the Blood-Brain Barrier and Kidney

Its Relevance to Salt-Induced Hypertension in Dahl Rats

Shlomoh Simchon; William Manger; Eugene Golanov; Jacob Kamen; George Sommer; Chris H. Marshall

From the Department of Medicine, Columbia University and New York University Medical Center, New York, NY.

Correspondence to Dr Shlomoh Simchon, National Hypertension Association, 324 E 30th St, New York, NY 10016.

Abstract—We previously reported that inappropriate renal vasoconstriction in Dahl salt-sensitive (DS) rats fed high NaCl diets may cause sodium retention. The present study examined the distribution and elimination of ²²Na in DS and Dahl salt-resistant (DR) rats, and we determined whether an abnormality in renal function might also cause sodium retention in DS rats. Following an intravenous bolus of 4 µCi ²²NaCl in prehypertensive DS and DR rats with similar blood pressures on low (0.23%) or high (8% for 4 days) NaCl diets, urinary clearance of ²²Na in 1 hour was about 4 times less in DS than DR rats, and renal retention of ²²Na was up to 8 times greater in DS than DR rats (P<0.01), suggesting that a renal functional defect may contribute to salt retention in DS rats; however, its uptake in tail artery, heart, lungs, liver, and spleen was similar in DS and DR rats. Uptake in brain was up to 5 times greater in DS than DR rats (P<0.01). Cerebrospinal fluid ²²Na radioactivity (in counts per minute) revealed that the blood-brain barrier is 5 to 8 times more permeable to sodium in DS than DR rats (P<0.01). Cerebrospinal fluid volume and brain water content increased significantly (P<0.01) in DS but not DR rats on an 8% NaCl diet. Intracerebroventricular bolus injection of 0.06 mL of 4.5 mol/L NaCl acutely and transiently induced the same degree of hypertension in DR and DS rats, whereas similar volume injections of isotonic saline, 4.5 mol/L Na-acetate, or 4.5 mol/L NaBr did not produce hypertension in either strain. We conclude that functional abnormalities in DS rat kidneys may cause retention of NaCl and that an increased blood-brain barrier permeability to NaCl may enhance its access to sites in the brain that are then activated and induce hypertension.

Key Words: brain • cerebrospinal fluid • hemodynamics • ventricles, cerebral • kidney • rats, Dahl

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