Preconditioning with sodium deficits to improve orthostatic tolerance in rats

We hypothesized that prior deficits in total body sodium would improve the subsequent ability of non-hypovolemic rats to maintain arterial pressure when subjected to an orthostatic challenge. This hypothesis was based on similarities in the response of neurohumoral cardiovascular control systems to lower-body negative pressure and negative sodium balance. Sodium deficits were induced in male Sprague-Dawley rats for 7-8 d by feeding sodium restricted diets, or by administering furosemide daily. After this, rats were allowed to regain a positive sodium balance for 1 d by increasing dietary intake or withholding furosemide, and receiving additional normal saline intraperitoneally. Rats subjected to these protocols had equal plasma volumes at the time they were anesthetized 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 position 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 furosemide treatment was associated with a higher peripheral resistance, while prior dietary restriction of sodium was associated with a higher cardiac output. We conclude that preconditioning consisting of chronic sodium deficits can improve orthostatic tolerance in this animal model. The hemodynamic data indicate the different modes of preconditioning may have their primary effect on different determinants of orthostatic tolerance.