The main pharmacological effects of iloprost, a stable prostacyclin (PGI(2)) derivative, are inhibition of platelet aggregation and vasodilatation, both effects being mediated by an activation of adenylate cyclase/cAMP complex. Na+ has an opposite, inhibiting adenylate cyclase effect on plasma membrane. The effect of iloprost (1 mu g/kg/min) was investigated on mean arterial pressure, bleeding time, in vivo platelet aggregation to collagen and plasma thromboxane A(2)/PGI(2) in genetically salt-sensitive Dahl rats (12) and their salt-resistant controls (12). In this subhypotensive dose, iloprost significantly increased bleeding time and plasma PGI(2) levels in both groups and significantly decreased TXA(2) levels. In vivo platelet aggregation to collagen was significantly inhibited in both groups. All described effects were more distinct in salt-sensitive, compared to salt-resistant rats (differences were significant). A modulation of Na+ effect by iloprost, via adenylate cyclase mechanism, was suggested.