Evidence against dopaminergic and further support for alpha-adrenergic receptor involvement in the pineal phosphatidylinositol effect.

Abstract

Abstract: Several α‐adrenergic receptor agonists and antagonists were used to strengthen the earlier findings that the stimulation by (‐)‐norepinephrine of 32P1 incorporation into acidic phospholipids, especially phosphatidylinositol, in the rat pineal gland is mediated through α‐adrenergic receptors. Dopamine was able to induce similar stimulation, although always to a smaller extent than equimolar concentrations of norepinephrine. The dopaminergic agonists apomorphine and piribedil did not increase phosphatidylinositol labeling. A number of antagonists considered to act primarily at dopaminergic or α‐adrenergic receptors respectively completely prevented dopamine from exerting its effect. Both types of antagonists also were able to inhibit in varying degree the elevation of phospholipid labeling induced by norepinephrine. Dopamine increased phosphatidylinositol turnover without first being converted to norepinephrine, inasmuch as dopamine β‐hydroxylase inhibitors had no influence on dopamine activity. Dopamine and α‐agonists competitively activated the receptors involved in the phospholipid effect. The conclusion drawn from the several lines of evidence is that only α‐adrenergic receptors are concerned with the changes in pineal phospholipid metabolism brought about by the various agonists used and that the action of dopamine occurs through these receptors rather than through discrete dopaminergic receptors.