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 μM NE, whereas maximal stimulation occurs at approximately 100 μM. Alpha1-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 alpha1-receptor antagonist, at a concentration of 0.05 μM inhibits 50% of the stimulation due to NE (100 μM), whereas 1 μM yohimbine, an alpha2-selective antagonist, is required to achieve the same effect. These results demonstrate the existence of an alpha1-adrenergic receptor-mediated PI effect in isolated canine cerebral microvessels.
|Original language||English (US)|
|Number of pages||5|
|State||Published - Jan 1 1983|