Propylthiouracil

About: Propylthiouracil is a research topic. Over the lifetime, 2181 publications have been published within this topic receiving 46996 citations. The topic is also known as: Thyreostat® & 2,3-dihydro-6-propyl-2-thioxo-4(1H)-pyrimidinone.

Ontogeny of beta-adrenergic receptors in the rat lung: effects of hypothyroidism.

Abstract: Beta-Adrenergic receptors were identified in membrane fractions of rat lung with the beta-adrenergic antagonists (-)-[3H]-dihydroalprenolol (-)-[3H]DHA) and (+/-)-[125I]-iodohydroxybenzylpindolol ((+/-)-[125I]HYP). Binding capacity (Bmax) for (-)-[3H]DHA increased progressively from 46 +/- 7 on day 18 of gestation to 510 +/- 70 femtomoles . mg-1 protein (mean +/- S.D.) on postnatal day 28, at which time adult Bmax was attained. An increase in (-)-[3H]DHA binding capacity of the lung was observed between postnatal days 15 and 28, during the known period of increased thyroid gland secretory activity, serum triiodothyronine (T3), and thyroxine (T4) concentrations in the rat. We therefore studied lung beta-adrenergic receptors in rat pups made hypothyroid with propylthiouracil (PTU) (in utero and postnatally) compared to normal age-matched control pups and to euthyroid pups which were treated with PTU but were also injected daily with thyroxine (T4-treated). Hypothyroid pups grew nearly normally until postnatal day 15 but grew poorly thereafter; but day 28 somatic and lung weight, lung DNA, and protein were markedly decreased in hypothyroid pups as compared to controls. Pulmonary beta-adrenergic receptors were similar in hypothyroid pups and controls on day 15, but were markedly decreased in hypothyroid pups on day 28 (294 +/- 57 versus 489 +/- 82 femtomoles . mg-1 protein in T4 treated euthyroid controls). Treatment of the hypothyroid pups with T4 on day 25 significantly increased lung beta-adrenergic receptors to near normal concentrations by day 28. We conclude that thyroid hormones or thyroid dependent factors enhance pulmonary beta-adrenergic receptor synthesis and that thyroid hormone is required for the normal postnatal maturation of the beta-adrenergic receptor system in the rat lung.

Effects of chronic ethanol administration on O2 consumption in whole body and perfused liver of the rat.

Abstract: The effects of chronic ethanol consumption on thyroid hormone levels and the rates of whole animal and perfused liver oxygen consumption were determined to test the hypothesis that alcoholic liver damage is a result of thyroid mediated liver hypermetabolism (L. Videla, J. Bernstein, and Y. Israel: Biochem. J, 134: 507–514, 1973). Whole animal minimal oxygen consumption, a sensitive indicator of the effects of thyroid hormone (W. D. Denckla: J. Clin. Invest, 53:572–581, 1974) was unchanged in rats maintained 3 wk on a liquid diet containing 34% of the calories as ethanol (2.49 ± 0.06 ml of O2/min/1O0 g of fat-free body weight) when compared to animals fed an equicaloric sucrose containing liquid diet (2.61 ± 0.20 ml of 02/min/100 g of fat-free body weight) or Purina chow (2.50 ± 0.12 ml of O2/min/100 g of fat-free body weight). Ethanol treatment lowered serum thyroxine (5.09 ± 0.20 pg/100 ml) compared to sucrose-fed control rats (7.66 ± 0.40 pg/100 ml), while serum triiodothyronine was unaffected (59.3 ± 4.0 compared to 66.9 ± 3.1 ng/100 ml for controls). Measurement of O2 consumption in the isolated perfused rat liver showed no significant difference after chronic treatment with the ethanol diet compared to either the sucrose or chow control diets. Infusion of 10-7 M norepinephrine into the perfusion medium resulted in an approximately 22% increase in O2 consumption in ethanol-fed animal and sucrose controls, while a 31 % increase was observed for sucrose-treated animals given 10 μg of T3/kg of body weight/day for 3 wk. These data indicate that T3 potentiates the ability of norepinephrine to increase O2 consumption. The data presented give no support to the concept that chronic ethanol ingestion results in hyperthyroidism or liver hypermetabolism and, consequently, the rationale for treatment of alcoholic hepatitis with the antithyroid drug, propylthiouracil, is incorrect (H. Orrego, H. Ka-lant, Y. Israel, et al.: Gastroenterology, 76:105–115, 1979).

Myxedema in the radiothyroidectomized dog.

Abstract: IN 1934 Trendelenburg, reviewing the early literature, stated that thyroidectomy in the dog results in a pronounced inhibition of skeletal growth in addition to other changes. In recent years, however, several reports have appeared (Danowski, Man and Winkler, 1946; Glock, 1949; Binswanger, 1936) indicating that the usual manifestations of hypothyroidism do not develop in dogs in which thyroid deficiency is induced either by surgical excision of the gland or by thiouracil administration. Even though Glock found an increased serum cholesterol as well as histological alterations in the thyroid and anterior hypophysis of thiouracil-treated dogs, she did not observe behavioral or myxedematous changes, growth impairment (puppies), or marked decline in metabolic rate. A striking study is that of Mayer (1947) who concluded “that beagles, and probably most dogs, do not need the thyroid function under ordinary conditions.” After administering propylthiouracil to pure-bred beagle puppies, he failed to observe any im...

Studies on the mechanism of hypothalamic control of thyrotropin secretion: effect of intrahypothalamic thyroxine injection on thyroid hypertrophy induced by propylthiouracil in the rat1

Abstract: A minute amount of thyroxine was injected into the anterior hypothalamus of rats chronically treated with propylthiouracil. The subsequent development of goiter was studied in relation to the hypothesis proposed in a previous paper that the “thyrotropin center” of the anterior hypothalamus is sensitive to alterations in the concentration of circulating thyroid hormone and thus can secondarily control thyrotropin secretion by the pituitary. The development of goiter was markedly inhibited by the injection of systemicalty ineffective amounts of thyroxine into the anterior hypothalamus but not by saline injections into the same area or by thyroxine injections into other areas of the hypothalamus. Adrenal and testicular weight were not affected by such procedures. It is suggested that thyroxine injection into the anterior hypothalamus specifically affects thyrotropin secretion by the pituitary.