Sequential changes of cerebrospinal fluid sodium during the development of hypertension in Dahl rats.

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Abstract
The role of sodium retention and consequent changes in cerebrospinal fluid sodium concentration in the genesis of hypertension in Dahl rats was evaluated. Dahl salt-sensitive (DS, n = 7), Dahl salt-sensitive (DR, n = 7), and Sprague-Dawley (n = 6) rats were housed in metabolic cages and instrumented wtih a stainless steel cannula in the cisterna magna and a femoral arterial catheter. A blood sample was drawn daily (200 .mu.l), and cerebrospinal fluid was collected by continuous 24-hour withdrawal (200 .mu.l/day). Daily sodium, potassium, and water balances were also determined. Rats were studied sequentialy on 0.4%, 4%, and 8% sodium diets (7 days per sodium level). Mean arterial pressure increased with 4% NaCl from 107 to 120 mm Hg (p < 0.05) over 24 hours in DS rats and remained at about that level until the NaCl was increased to 8%, which resulted in a gradual rise of mean arterial pressure over the next 7 days to 135 mm Hg. Cerebrospinal fluid sodium was unchanged in DR and Sprague-Dawley rats fed 4% or 8% sodium, but in DS rats rose from 152.3 to 155.2 .+-. 0.6 meq/l on the third day at 4% sodium and remained elevated over the next 2 weeks of study. Blood sodium was unchanged throughout the study in all groups. On the first day only the 4%and 8% sodium diets, both DS and DR rats exhibited a similar net retention of sodium, which was greater than the Sprague-Dawley rats (p < 0.05). There was no evidence for greater retention of sodium or water, however, in DS rats compared with DR or Sprague-Dawley rats when subjected to a high sodium diet. In summary, since mean arterial pressure rose in DS rats on the first day of the 4% sodium diet while cerebrospinal fluid sodium did not change until the third or fourth day, we conclude that these central changes were not the stimulus for the initial rise of arterial pressure but might contribute to the maintenance of the hypertension.