Role of aldosterone in stress-induced antinatriuresis in normotensive saline overload rats

The aim of this study was to determine aldosterone participation in the stress-induced antinatriuresis in normotensive saline overload rats, as a probable cause of stress-induced hypertension. Spironolactone (Sp) 6 mg/kg/day, intraperitoneal injection, as a Mineralocorticoid receptor antagonist was used. The rats were divided into four groups: basal (B), basal drug (B-Sp), stress [Immobilization stress (IMO)] and stress-Sp (IMO-Sp). Urinary Na+ and K+ were measured and the K+/Na+ ratio was calculated. Aldosterone and corticosterone plasmatic levels were determined. Stressed rats showed higher aldosterone and corticosterone levels than the ones in the basal group. The antinatriuretic effect in response to acute IMO was not reverted with Sp. However, IMO-Sp animals sbowed higher urinary sodium levels than IMO animals suggesting a partial inhibition of the stress response. The IMO-Sp animals excreted SO per cent of basal sodium while IMO animals excreted about 20 per cent of B sodium. This effect was also evidenced in the urinary K+/Na+ ratio. In conclusion, aldosterone would be a factor influencing sodium reabsorption in stressed rats. Since sodium distal handling is small with respect the proximal ones, in which the sympathetic innervation is great, the inhibition of aldosterone action is not enough to revert antinatriuretic effect. Besides, the high levels of corticosterone might exert some effect on stressinduced antinatriuresis. These results show the importance of aldosterone in the sodium reabsorption in IMO rats as a contributing factor to explain the origin of stress-induced hypertension in rats. Copyright (c) 2008 John Wiley & Sons, Ltd.