Handling (NaCl)-Na-22 by the blood-brain barrier and kidney - Its relevance to salt-induced hypertension in Dahl rats

We previously reported that inappropriate renal vasoconstriction in Dahl sa lt-sensitive (DS) rats fed high NaCl diets may cause sodium retention. The present study examined the distribution and elimination of Na-22 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 i ntravenous bolus of 4 mu Ci (NaCl)-Na-22 in prehypertensive DS and DR rats with similar blood pressures on low (0.23%) or high (8% for 4 days) NaCl di ets, urinary clearance of Na-22 in 1 hour was about 4 times less in DS than DR rats, and renal retention of Na-22 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, l ungs, 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 Na-2 2 radioactivity (in counts per minute) revealed that the blood-brain barrie r is 5 to 8 times more permeable to sodium in DS than DR rats (P<0.01). Cer ebrospinal fluid volume and brain water content increased significantly (P< 0.01) in DS but not DR rats on an 8% NaCl diet. Intracerebroventricular bol us injection of 0.06 mL of 4.5 mol/L NaCl acutely and transiently induced t he same degree of hypertension in DR and DS rats, whereas similar volume in jections of isotonic saline, 4.5 mol/L Na-acetate, or 4.5 mol/L NaBr did no t produce hypertension in either strain. We conclude that functional abnorm alities 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 i n the brain that are then activated and induce hypertension.