Effects of alpha-trinositol administered extra- and intracellularly (using liposomes) on rat aorta rings.

The effects of alpha-trinositol, a D-myo-inositol [1,2,6]trisphosphate derivative, were studied on de-endothelised rat aorta rings. The substance was applied extracellularly as well as intracellularly (by using liposomes as drug carriers). Upon extracellular administration, the drug reduced the level of contraction induced by 40 mM K+ or by phenylephrine (10(-5) M). No effects were observed on relaxed preparations. Liposomes containing alpha-trinositol induced a dose-dependent contraction of the preparations under resting tension with a threshold of 10(-5) M in the aqueous phase. These contractions were heparin-insensitive but were significantly blocked by D-600 (10(-5) M) (an L-type Ca2+ channel blocker) or in Ca(2+)-free medium. Our data suggest that alpha-trinositol has a plasmalemmal mechanism of action which could involve Ca2+ influx from the extracellular space.