1. In corticosterone-induced hypertension in rats the activity of the peripheral sympathetic nervous system and its modulation by prostaglandins was studied.
2. Plasma concentrations of noradrenaline were reduced if compared with those in normotensive control rats.
3. The sensitivity of the isolated perfused hindlimb preparation to noradrenaline was enhanced before blood pressure rose and increased further with the development of hypertension.
4. Arachidonic acid, prostacyclin (prostaglandin I2), but not 6-keto-prostaglandin F1α, reversed the supersensitivity to noradrenaline.
5. These results suggest that corticosterone induces a supersensitivity to noradrenaline by inhibiting the biosynthesis of prostaglandins. Changes in the sensitivity of the vascular smooth muscle may play a role in the development of glucocorticoid hypertension.