Stimulation of the phosphoinositide signalling system as a possible mechanism for glucocorticoid action in blood pressure control

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Abstract
Cortisol stimulates the phosphoinositide signalling system in smooth muscle cells of the rat aorta. After stimulation of the cells with cortisol, epinephrine or both compounds, inositol-1,4,5-trisphosphate concentrations were analysed by standardized ionexchange chromatography procedure. A 15-min stimulation with physiological concentrations of cortisol (0.02–5.0 μg/ml) led to a dose-dependent increase of the inositol trisphosphate concentrations (up to 500%) and also to a translocation of the calcium-and lipid-dependent protein kinase C activity from the cytosolic to the membranous compartment. Incubation of smooth muscle cells with epinephrine (10-9 to -5 mol/l) did not lead to an increase in the inositol trisphosphate concentrations. However, after pre-incubation with an average dose of cortisol (0.2 μg/ml) the inositol trisphosphate response was potentiated by 10-7 mol/l epinephrine. Our results suggest that stimulation of the phosphoinositide system is a still unknown mechanism of glucocorticoid action in smooth muscle cells, which could influence intracellular free calcium and thus vascular reactivity and blood pressure.

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