[Effects of aldosterone and vasopressin on transmembrane efflux of sodium from the arterial wall].

We have previously shown that, injected s.c. to adrenalectomized Sprague-Dawley rats (SD.ADx), aldosterone has a mineralocorticoid specific effect on transmembrane movements of 22Na from arterial smooth muscle. These effects appear to be partly due to the action of an humoral factor. Indeed, in vitro, the late increase in passive 22Na efflux is not observed (Moura and Worcel, 1984). In rats perfused with a specific antagonists of the pressor effect of vasopressin (Vp), the in vivo administration of aldosterone induced a kinetic action similar to that observed after in vitro exposure to the mineralocorticoid. These results suggested that Vp may be the humoral factor (Moura, Angeli and Worcel, 1985). In adrenalectomized homozygous Brattleboro rats (DI.ADx), aldosterone (10(-8)M) increases ouabain independent 22Na efflux (DI.AX: 0.073 +/- 0.002 min-1(n = 15); DI.ADx + Aldo: 0.096 +/- 0.002 min-1(n = 12)p less than 0.01) and ouabain-dependent 22Na efflux (DI.ADx: 0.031 +/- 0.001 min-1; DI.ADx + Aldo: 0.037 +/- 0.002 min-1 p less than 0.01). Vp also increases ouabain sensitive and insensitive 22Na effluxes and potentiates the effects of aldosterone on passive Na+ transferts (DI.ADx + Aldo + Vp: 0.015 +/- 0.003 min-1 (n = 16) p less than 0.01). In conclusion, these results suggest that Vp may be involved in the effects of aldosterone on 22Na effluxes. Furthermore Vp potentiates the effects of aldosterone on passive 22Na effluxes. But it is not yet possible to ascertain if Vp action is additive or permissive.