An alpha1-adrenergic receptor-mediated phosphatidylinositol effect in canine cerebral microvessels.

In microvessels isolated from canine cerebral cortex, 32Pi is incorporated into phospholipids when incubated in physiological buffer containing [32Pi]orthophosphate. Norepinephrine (NE) selectively increases 32Pi incorporation into phosphatidylinositol (PI) and phosphatidic acid (PA) 60-200% over control levels. Half-maximal stimulation of PI labeling is observed with 1 microM NE, whereas maximal stimulation occurs at approximately 100 microM. Alpha 1-adrenergic agonists, phenylephrine and methoxamine, mimic the effects of NE, whereas isoproterenol, a beta-adrenergic receptor agonist, is ineffective. A wide variety of other agents tested had no specific effect on 32Pi incorporation into PI or PA. Prazosin, a selective alpha 1-receptor antagonist, at a concentration of 0.05 microM inhibits 50% of the stimulation due to NE (100 microM), whereas 1 microM yohimbine, an alpha 2-selective antagonist, is required to achieve the same effect. These results demonstrate the existence of an alpha 1-adrenergic receptor-mediated PI effect in isolated canine cerebral microvessels.