Inhibition of TSH-stimulated thyroid hormone release and potentiation of TRH-stimulated TSH release by indomethacin in perifusion systems of rat thyroids and pituitaries

Summary Using indomethacin (Ind), a prostaglandin, synthesis inhibitor, in vivo experiments in rats and in vitro experiments with perifusion systems of rat thyroids and pituitaries were conducted. After 35 days of intragastric infusion of Ind, serum TSH levels were markedly increased, the thyroid was swollen and, as a consequence, T₃ and T₄ levels were normal. The T₃ release from perifused rat thyroids under continuous stimulation with 10 mU/ml TSH was inhibited significantly (p<0.01) by 1.0×10^–6 M Ind. On the other hand, the TSH release from perifused rat pituitaries under TRH stimulation was enhanced conspicuously by Ind. It was concluded that Ind decelerated thyroid hormone release from the thyroid and accelerated TSH release from the pituitary in perifusion systems.     

Release of 3,5,3'-triiodothyronine, thyroxine and thyroglobulin from TSH-stimulated mouse thyroids in the perifusion system

We established a perifusion system using mouse thyroid glands. In this system, TSH increased the release of T3 and T4 significantly, and the response of thyroglobulin to TSH was delayed in comparison with that of T3 and T4.     

Release of 3,5,3′-triiodothyronine,thyroxine and thyroglobulin from TSH-stimulated mouse thyroids in the perifusion system

Summary We established a perifusion system using mouse thyroid glands. In this system, TSH increased the release of T₃ and T₄ significantly, and the response of thyroglobulin to TSH was delayed in comparison with that of T₃ and T₄.     

Effect of sulpiride on prolactin release by rat pituitaries in vitro

Résumé La sulpiride stimule la libération de la prolactine de l'hypophise après 4 h d'incubation. L'addition d'extraits hypothalamiques l'inhibe, mais la sulpiride ajoutée en même temps aux extraits hypothalamiques permet l'inversion de cet effet d'inhibition. Il semble evident que la sulpiride peut modifier la libération de la prolactine en agissant directement sur l'hypophise du rat, in vitro.     

Effect of thyroid hormone on somatomedin-C release from perfused rat liver

The effect of thyroid hormone on plasma somatomedin-C (SmC) level and on SmC release from perfused rat liver was investigated. Plasma SmC levels and liver tissue SmC were significantly increased in thyroxine-treated rats. Physiological doses of triiodothyronine increased SmC release and SmC concentration in the perfused rat liver. These results indicate that thyroid hormone directly enhances the synthesis and release of SmC in the rat.     

Inhibition of endogenous TSH in rats by antiserum to bovine TSH

Riassunto Gli autori hanno ottenuto in conigli un siero anti-TSH usando come antigene ormone bovino. Questo siero inibisce il TSH endogeno di ratti nutriti con dieta di Remington e trattati con tiouracile, impedendo cosi la formazione della iperplasia tiroidea. È stato anche osservato che il trattamento con siero anti-TSH mantiene normale il rapporto MIT/DIT cancellando le salienti alterazioni indotte dal trattamento con tiouracile.     

Differences in luteinizing hormone release stimulated in rat anterior pituitary cells by leukotriene C4 and by gonadotropin-releasing hormone in vitro

Continuous administration of leukotriene C4 (LTC4, 10(-10) M) to superfused rat anterior pituitary cells increased LH release for 40 min only, whereas in a parallel experiment gonadotropin-releasing hormone (GnRH, 10(-9) M) evoked a continuous increase in hormone secretion. In contrast to GnRH, LTC4 did not desensitize rat anterior pituitary cells. The secretory action resulting from the administration of LTC4 (10(-10) M) was abolished for 40 min after previous stimulation. The results documented the dual action of LTC4 on LH exocytosis.     

Differences in luteinizing hormone release stimulated in rat anterior pituitary cells by leukotriene C4 and by gonadotropin-releasing hormone in vitro

Summary Continuous administration of leukotriene C₄ (LTC₄, 10^–10 M) to superfused rat anterior pituitary cells increased LH release for 40 min only, whereas in a parallel experiment gonadotropin-releasing hormone (GnRH, 10^–9 M) evoked a continuous increase in hormone secretion. In contrast to GnRH, LTC₄ did not desensitize rat anterior pituitary cells. The secretory action resulting from the administration of LTC₄ (10^–10 M) was abolished for 40 min after previous stimulation. The results documented the dual action of LTC₄ on LH exocytosis.     

Effect of a fraction of bovine hypothalamic extract on the release of TSH by rat adenohypophysesin vitro

Zusammenfassung Die elektrophoretisch isolierte Franktion des hypothalamischen Extraktes erhöhtin vitro die Sekretion des thyreotropen Hormons aus der Adenohypophyse der Ratte in der Krebs-Phosphat-Ringerlösung mit 300 mg% Glukose. Die Fraktion selbst besitzt keine TSH-Wirkung.     

Somatostatin inhibits in vitro release of luteinizing hormone releasing hormone from rat mediobasal hypothalamic slices

Summary Somatostatin, in concentrations ranging from 10^–10 M to 10^–7 M, induces a dose-dependent inhibition of LHRH release from mediobasal hypothalamic slices incubated in vitro. In contrast, VIP, secretin, glucagon, substance P, neurotensin and arginine-vasotocin do not affect spontaneous release of LHRH.     

Antidiuretic hormone involvement in the release of alpha-melanocyte-stimulating hormone by hyperosmotic stimuli

In the normal Wistar rat, the plasma alpha-MSH level was raised by hypertonic saline injection (as compared with control rats injected with isotonic saline). No such rise in alpha-MSH followed hypertonic saline administration in the Brattleboro (hereditary diabetes insipidus) animal (compared to isotonic saline injected controls). It is suggested that, in the rat, endogenous antidiuretic hormone is involved in the secretory response of the pars intermedia to osmotic stimuli.     

Inhibition of LH-RH induced release of gonadotropins by substance P in cultured rat anterior pituitary cells]

Using anterior pituitary cells cultured for 7 days and then incubated for 4 hrs, substance P, an undecapeptide, inhibited the stimulatory effect of LH-RH on the release of LH-RH on the release of LH and FSH. This inhibitory effect, which was similar for both gonadotropins was only observed when the adenopituitary cells were put in culture at DI and Proestrus stages of the oestrous cycle. Furthermore substance P partly inhibited the basal release of FSH at DI and DII stages but did never affected that of LH.     

Induction of hyperlipidemia by human thyroid stimulating hormone immunization in rabbits

Summary In our study we are able to demonstrate that with TSH booster and bleeding animals 10–20 days post immunization, when rabbits have increased in antibody titer, there is an increase in cholesterol and triglyceride. These findings are suggestive that most probably we are rendering these rabbits hypothyroid.Acknowledgments. The authors are indebted to Miss J. Meister for her skillful technical help. We are also indebted to the National Institute of Arthritis, Metabolism, and Digestive Diseases for Human Thyroid Stimulating Hormone for iodination.     

Inhibition of food intake in the rat by cyproheptadine

Summary In a model of conditioned feeding behavior, oral administration of cyproheptadine (1–100 mg/kg), 30 min before presentation of food, produced a dose-dependent reduction of food intake in the rat (ED₅₀17 mg/kg during the 1st h of testing). This anorexic effect persisted for at least 24 h. These results provide further evidence that under certain conditions cyproheptadine, which is used as an orectic agent in man, can produce anorexia.     

Inhibition of saline-induced diuresis in the rat by sulpiride

Summary Sulpiride (120 mg/kg, i.p.) inhibited saline-induced diuresis in the rat, an effect not observed with haloperidol, clozapine, pimozide or chlorpromazine. The antidiuretic effect of sulpiride also occurred in hypophysectomized rats suggesting that the response was not prolactin-mediated.     

Inhibition of platelet ADP and serotonin release by carbon monoxide and in cigarette smokers

Summary The release of¹⁴C-serotonin by ADP, epinephrine and arachidonic acid and the release of ADP by kaolin were measured in normal platelets in the presence and absence of carbon monoxide and in smokers' platelets. It is shown that carbon monoxide inhibits significantly the platelet release reaction. This function is also decreased in platelets obtained from heavy cigarette smokers.This work was supported by Veterans Administration Research Fund 8073-01.