Brain ‘Ouabain’ and Desensitization of Arterial Baroreflex by High Sodium in Dahl Salt-Sensitive Rats

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Abstract
Abstract In Dahl salt-sensitive (S) rats, high sodium intake further desensitizes arterial baroreflex function. To assess the possible involvement of brain “oubain,” we gave Dahl S rats a regular or high sodium diet from 4 to 7 weeks of age and administered intracerebroventricular antibody Fab fragments, which bind ouabain with high affinity, or γ-globulins as control (200 μg/12 μL per day for both) using osmotic minipumps. We assessed arterial baroreflex function by plotting changes in renal sympathetic nerve activity or heart rate against changes in mean arterial pressure of conscious rats elicited by intravenous phenylephrine and nitroprusside. Dahl S rats on high sodium treated with γ-globulins showed a significantly higher resting mean arterial pressure versus other rats (130 to 140 versus 95 to 105 mm Hg). In rats treated with γ-globulins, high sodium desensitized baroreflex control of renal sympathetic nerve activity compared with rats on regular sodium (average gain: −1.88±0.12 versus −2.73±0.13, P <.05). In contrast, in rats treated with Fab fragments, high sodium did not increase blood pressure and did not desensitize but slightly sensitized reflex control of renal sympathetic nerve activity. Changes in reflex control of heart rate were similar to those of renal sympathetic nerve activity. These data indicate that blockade of brain “oubain” prevents sodium-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 Dahl S rats on high sodium.