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The chromatophorotrophic effect of ACTH which, in the Addisonian patient does not require the presence of the adrenal glands, has been studied in the tree frog (Hyla arborea).
Frog skin in vitro gave the chromatophorotrophic effect with solutions of ACTH. Slight reactions were produced by intermedin, pitressin and pitocin, while fifteen other hormones and thirty-eight amines gave negative reactions. There was a conspicuous difference between the effective concentration of ACTH in vivo and in vitro, the doses required for the in vitro effect being about a thousand times higher.
Adrenalectomized, hypophysectomized, as well as intact frogs showed the full chromatophorotrophic effect.
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Six groups each of 12 male albino rats were reared from day 21 of life at temperatures of 23, 34 or 37 °C. While the rats survived for unlimited periods at 23 and 34 °C, the animals reared at 37 °C succumbed within 5 days to heat stress. The latter group, when injected s.c. or i.p. with 50 mg dehydroepiandrosterone (DHA)/kg/day were no longer affected by the heat. During this treatment thyroid epithelial cell height doubled, colloid decreased by 20%, connective tissue did not change, the basic metabolic rate decreased by 10% and rectal temperatures of the treated rats increased with the ambient temperatures. Body weight increased only slightly, pituitary TSH decreased by 25%, serum TSH increased by over 50%, thyroxine and 125I uptake increased by 200%. The survival of the DHA-treated rats was apparently secured by blocking the hypothalamic thermoreceptors.
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The negative feedback action of the hypothalamic—hypophysial—thyroid system is abolished in rats kept at 37 °C, presumably due to the stress of the high temperature (Weller, Dikstein & Sulman 1969; Tal & Sulman, 1971). The present investigation compares pituitary thyroid-stimulating hormone (TSH) levels in rats kept at room temperature (23 °C) or at higher temperatures (34 °C or 37 °C).
Six groups of 12 male albino rats of the Hebrew University Sabra strain, 42 days old and weighing 120 ± 5 g each, were housed six to a cage in three rooms at 23 ± 1 °C, 34 ± 1 °C and 37 ± 1 °C respectively. The rats received standard laboratory pellets and water ad libitum. Synthetic thyrotrophin releasing factor (TRF) (300 ng/kg body wt) (pyroglutamyl-histidyl-prolinamide, Farbwerke Hoechst A.G., Frankfurt) was injected i.v. (Kendall, Rees & Kramer, 1971) on the 4th day in the experimental groups. The rats were
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Dehydroepiandrosterone (DHA), a weak androgen with a potency one-fifth of that of testosterone, stimulates thyroid activity (Tal & Sulman, 1972). The mechanism of this effect is studied in the present paper.
DHA (1, 5, 10, 20 or 50 mg/kg/day) was administered daily i.p. to 21-day-old male rats of the Hebrew University Sabra strain. The rats received standard Purina chow and water ad libitum, were kept in a room at 23 ± 1 °C with artificial lighting for 12 h daily, and were killed after 21 days of treatment. DHA was also implanted stereotaxically (Mess, 1967) in the anterior basal hypothalamus of 42-day-old male rats (5 μg/rat), the pellets being ejected into the tissue from Rudmond's disposable glass micro-tubings and their location later confirmed histologically. The site chosen was A = 0, L = 0, H = -8 (König & Klippel, 1963). The rats were killed by decapitation 4, 24, 48 or 72 h
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Radioactive [14C]5-hydroxytryptamine (5-HT, serotonin) creatinine sulphate was injected intrapleurally into female rats treated with oestrogen and/or progesterone which had received, immediately before the injection of 5-HT, homogenates of placenta, foetus, uterus or plasma, taken from pregnant rats on the 19th day of pregnancy. The placental homogenate produced a significant increase in 5-HT uptake by the myometrium, when the rats had been primed with moderate doses of oestrogen plus progesterone. Higher doses prevented the increased uptake, and oestrogen treatment alone did not induce 5-HT uptake. The highest level of 5-HT accumulation in the uterus was produced by placental extract after pretreatment with 0·5 mg. oestradiol plus 10 mg. progesterone/rat/day.
These results suggest that the placenta contains a 'trans-serotonin' system which is dependent on the oestrogen—progesterone balance and serves to accumulate 5-HT in the placenta and myometrium. Shifts of the hormonal balance may contribute to the release of 5-HT and thus promote uterine contractions at any stage of pregnancy.
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Intra-aortic injection of [3-14C]5-hydroxytryptamine creatinine sulphate ([14C]5-HT) into oestrogen or oestrogen-progestogen treated rats showed a pattern of homogeneous uptake similar to that found in untreated normal rats. In pregnant rats the injection resulted in a preferential uptake by the myometrium. Injection of a MAO inhibitor (pargyline hydrochloride, Eutonyl) into the amniotic sac, preceding the [14C]5-HT injection by 30 min., changed this pattern to a preferential accumulation in the myometrium and the spleen, perhaps due to unhampered transport of preserved 5-HT by the thrombocytes to the spleen. When [14C]5-HT was injected i.p. into the foetuses they retained high amounts of exogenous 5-HT. Myometrium and placenta also showed increased 5-HT uptake.
This finding—taken together with the established fact that foetal 5-HT increases and placental monoamine oxidase decreases steadily up to term—suggests that at term the release of foetal 5-HT may enrich the maternal myometrium with 5-HT through the umbilical arteries without its entering the general blood circulation. It is also possible that additional maternal 5-HT may accumulate in the myometrium sensitized by the oestrogen surge at term. The importance of these mechanisms for the induction of labour is discussed.
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The monoamine oxidase inhibitor mebanazine (Actomol) was found to reduce the growth of cartilage, and the normal increase in body weight and pituitary weight in growing male rats. The inhibitory effect of mebanazine on cartilage growth is only partially overcome by concomitant injection of growth hormone. The inhibitory effect on growth is much greater when mebanazine is injected together with hydrocortisone; it exceeds by far the sum of the effects of mebanazine or hydrocortisone alone (augmentative synergism).
Mebanazine also inhibits cartilage growth in normal rats receiving metyrapone (Metopirone—which inhibits corticosteroid production) and in adrenalectomized animals receiving hydrocortisone. Mebanazine stimulates involution of the thymus and depletion of ascorbic acid from the adrenal glands of rats. This shows that mebanazine releases adrenocorticotrophic hormone in normal rats and in rats receiving high doses of hydrocortisone.
Our results thus suggest that the inhibitory effect of mebanazine on growth is twofold: it potentiates a corticosteroid which itself is a growth inhibitor and in addition blocks the release of growth hormone from the pituitary by a specific mechanism inherent in the action of mebanazine as an enzyme blocker.
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A large number of monoamine oxidase (MAO) inhibitors: pivhydrazine (Tersavide), nialamide (Niamide), isocarboxazid (Marplan), mebanazine (Actomol), phenelzine (Nardil), pheniprazine (Catron) and tranylcypromine (Parnate), decrease cartilage growth in normal rats. This inhibition is not directly due to their properties as MAO inhibitors. Thus, for example, iproniazid (Marsilid), 2,5-dichlorophenylhydrazine, etryptamine (Monase) and amphetamine (Benzedrine) did not decrease epiphysial growth of the tibia in immature female rats. MAO inhibitors with a methyl residue on the α-carbon atom inhibited growth to a greater extent than those with a hydrogen in place of the methyl group.
Pargyline (Eutonyl) did not depress cartilage growth in adrenalectomized rats, even when they received large doses of adrenaline. However, pargyline inhibited cartilage growth in adrenalectomized animals receiving hydrocortisone and in normal rats. Thus the growth-inhibiting effect of pargyline seems to be mediated by its potentiating effect on corticosteroids.
Growth hormone prevented the inhibitory effect of pargyline on cartilage growth. Pargyline alone given to normal young male or female rats decreased weight gain for 2 weeks. Later the experimental animals caught up with the controls. It is assumed that the transient weight loss is due to the sympathomimetic effect of the MAO inhibitor, which depresses hypothalamic centres concerned with appetite, weight gain and growth.
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The mechanism by which combined treatment with monoamine oxidase inhibitors and a corticosteroid reduces the weight of the accessory sex glands in intact rats by about one half has been studied. Phenelzine sulphate in combination with hydrocortisone acetate given for 30 days to ovariectomized rats reduced the pituitary stores of luteinizing hormone (LH) by 33%. Similar reductions in somatotrophic hormone, corticotrophin and thyroid-stimulating hormone content were found after comparable treatment, whereas luteotrophic hormone increased.
The increase of weight of the seminal vesicles and prostate gland produced by human chorionic gonadotrophin could be partly antagonized by the simultaneous administration of mebanazine and dexamethasone, but the action of testosterone on these glands in castrated animals was not inhibited. Interference with the production and effectiveness of LH is therefore the most likely mode of action by which these drugs effect the reduction of the weight of the accessory sex glands.
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Recent reports on the in-vivo and in-vitro effects of the β-adrenergic blocking agent propranolol (Inderal, I.C.I.) (Burke, 1969; Franco, 1970; Melander, 1971; Biran & Tal, 1972) have arrived at contradictory conclusions regarding its effect on thyroid activity. The present paper is devoted to clarification of this problem in vivo by investigating: (a) the influence of propranolol on thyroid secretion, (b) the direct or indirect effect of propranolol on the thyroid gland, and (c) involvement of the hypothalamus—pituitary system.
Intact rats.
Propranolol (1–5 mg/kg) was administered daily i.p. in 0·1 ml propylene glycol to 32 male 21-day-old rats of the Hebrew University Sabra strain, weighing 42 ± 2 g. The rats were divided into four equal groups (nos. 1–4) and received standard Purina chow and water ad libitum. The cages were kept at 23 ± 1 °C and exposed to artificial light for 12 h daily. On the 42nd day of life the
