PRECONDITIONING WITH SODIUM DEFICITS TO IMPROVE ORTHOSTATIC TOLERANCEIN RATS

We hypothesized that prior deficits in total body sodium would improve the subsequent ability of non-hypovolemic rats to maintain arterial p ressure when subjected to an orthostatic challenge. This hypothesis wa s based on similarities in the response of neurohumoral cardiovascular control systems to lower-body negative pressure and negative sodium b alance. Sodium deficits were induced in male Sprague-Dawley rats for 7 -8 d by feeding sodium restricted diets, or by administering furosemid e daily. After this, rats were allowed to regain a positive sodium bal ance for 1 d by increasing dietary intake or withholding furosemide, a nd receiving additional normal saline intraperitoneally. Rats subjecte d to these protocols had equal plasma volumes at the time they were an esthetized and evaluated for orthostatic tolerance. Furosemide-treated rats maintained a higher mean arterial pressure (MAP) than controls ( 70 +/- 10 vs 34 +/- 9 mm Hg) when rotated to a 90 degrees head-up posi tion for 20 s. Rats receiving the lowest dietary sodium maintained the highest MAP (89 +/- 8 mm Hg) when placed at 60 degrees head-up for 5 min. Both before and during the orthostatic challenges, prior furosemi de treatment was associated with a higher peripheral resistance, while prior dietary restriction of sodium was associated with a higher card iac output. We conclude that preconditioning consisting of chronic sod ium deficits can improve orthostatic tolerance in this animal model. T he hemodynamic data indicate the different modes of preconditioning ma y have their primary effect on different determinants of orthostatic t olerance.