BRAIN OUABAIN AND DESENSITIZATION OF ARTERIAL BAROREFLEX BY HIGH SODIUM IN DAHL SALT-SENSITIVE RATS

In Dahl salt-sensitive (S) rats, high sodium intake further desensitiz es arterial baroreflex function. To assess the possible involvement of brain ''oubain,'' we gave Dahl S rats a regular or high sodium diet f rom 4 to 7 weeks of age and administered intracerebroventricular antib ody Fab fragments, which bind ouabain with high affinity, or gamma-glo bulins as control (200 mu g/12 mu L per day for both) using osmotic mi nipumps. We assessed arterial baroreflex function by plotting changes in renal sympathetic nerve activity or heart rate against changes in m ean arterial pressure of conscious rats elicited by intravenous phenyl ephrine and nitroprusside. Dahl S rats on high sodium treated with gam ma-globulins showed a significantly higher resting mean arterial press ure versus other rats (130 to 140 versus 95 to 105 mm Hg). In rats tre ated with gamma-globulins, high sodium desensitized baroreflex control of renal sympathetic nerve activity compared with rats on regular sod ium (average gain: -1.88+/-0.12 versus -2.73+/-0.13, P<.05). In contra st, in rats treated with Fab fragments, high sodium did not increase b lood pressure and did not desensitize but slightly sensitized reflex c ontrol of renal sympathetic nerve activity. Changes in reflex control of heart rate were similar to those of renal sympathetic nerve activit y. These data indicate that blockade of brain ''oubain'' prevents sodi um-induced hypertension as well as the desensitization of the arterial baroreflex in Dahl S rats. Increased brain ''oubain'' may desensitize the arterial baroreflex and thereby facilitate the hypertension in Da hl S rats on high sodium.