An alpha1-adrenergic receptor-mediated phosphatidylinositol effect on canine cerebral microvessels

R. J. Zeleznikar, E. E. Quist, Lester R Drewes

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24 Scopus citations


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 languageEnglish (US)
Pages (from-to)163-167
Number of pages5
JournalMolecular Pharmacology
Issue number1
StatePublished - Jan 1 1983


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