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The circadian pattern of LH release observed in ovariectomized estrogen-implanted rats was inhibited by blockade of alpha-adrenergic receptors by phenoxybenzamine; in contrast, blockade of beta-receptors by propranolol was ineffective. Prasozin, an alpha 1-antagonist, was as effective as phenoxybenzamine, whereas yohimbine, an alpha 2-antagonist, was effective only at high doses. Neither phenoxybenzamine nor prazosin were able to modify the LHRH-induced release of LH from superfused pituitaries. These results suggest an involvement of hypothalamic alpha 1-receptors in the control of circadian LH release.

The present experiment investigated changes in pituitary-adrenal activity, prolactin and catecholamine synthesizing enzymes in rats exposed to electric shocks in pairs or individually, in comparison to animals receiving no shock and tested in pairs or alone. Pairs of rats repeatedly exposed to electric shocks displayed a lower activation of the pituitary-adrenal system but a stronger activation of the sympathetic-adrenal medullary system than rats shocked individually. There was no differential release of prolactin according to the social setting in which shock occurred. Social factors by themselves influenced plasma corticosterone levels but not plasma levels of ACTH and prolactin nor catecholamine synthesis. The results are discussed in relation to the postulated beneficial effects of fighting on physiological activation produced by electric shock.