No abstract

³H-Oestradiol uptake by the median eminence, anterior pituitary, and uterus of ovariectomized albino rats is significantly reduced when the hormone is injected after i.v. administration of perphenazine, while its uptake in the cerebral cortex is not affected by perphenazine. The most pronounced competition is noted 30 min after the oestradiol injection: it lasts 60 min in the median eminence, but more than 2 h in the anterior pituitary, where the ³H-oestradiol uptake is 10 times higher. The peak of ³H-oestradiol radioactivity in the different organs is reached in the median eminence and cerebral cortex 15 min after injection, in the anterior pituitary after 2 h, and in the uterus more than 3 h afterwards. A decline in the ³H-oestradiol uptake is observed in the median eminence; but in the anterior pituitary it rises steadily for up to 2 h. Increasing the perphenazine-priming dose yields a dose-response curve of decreased ³H-oestradiol uptake. The fact that aminopromazine and phenothiazine are also able to partly saturate the binding receptors of oestradiol in its target-organs points to specific receptor competition. This may explain some of the central endocrine effects exerted by phenothiazines.

Nitroglycerin was traced in the blood of 20 patients up to 4 h after oral administration of a sustained release preparation (Nitro-Mack Retard). The determination needs an extremely sensitive method using GLC-columns with 3% SE-30 (Packard) equipped with an electron capture detector.

No abstract

The capacity of the pigeon pituitary gland to release prolactin was investigated in vivo, to evaluate its hypothalamic regulation and to establish the dominant hypothalamic factor for prolactin secretion. After 3 days of systemic administration of some physiological and pharmacological agents, followed by 2 consecutive days of local intradermal injections of prolactin into their crop sacs, the crop mucosa was scraped, dried and weighed. The substances tested were: oestradiol and tamoxifen (antioestrogen), thyrotophin-releasing hormone (TRH) and anti-TRH serum, perphenazine (releases prolactin in mammals) and bromocriptine (suppresses prolactin in mammals). Prolactin and anti-prolactin serum were tested as controls. While prolactin markedly proliferated and anti-prolactin serum significantly inhibited the mucosal weight, oestradiol, TRH and perphenazine dramatically depressed proliferation of the mucosa, suggesting that prolactin secretion was inhibited. Tamoxifen, anti-TRH serum and bromocriptine significantly increased the proliferation of the crop mucosa, indicating an increase in the endogenous release of prolactin. Since the effect of these substances on prolactin release in the pigeon is the opposite from their well-established effects in mammals, these results suggest, in a specific and homologous model, that the dominating regulator for prolactin in the pigeon is contrary to that in the mammal, namely prolactin-releasing factor, and that TRH may play a significant role in the physiological regulation of prolactin secretion.