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Notes: 1. The anti-thyroid drug, propylthiouracil (0.05% w/v in drinking water) was administered to rats for 3–4 weeks. This treatment decreased the rate at which rats gained body weight but did not affect the weight of the vasa deferentia. Circulating levels of thyroxine and triiodothyronine were markedly decreased.2. The potencies of postjunctional α-adrenoceptor agonists, 1-noradrenaline and 1-phenylephrine, in eliciting contraction of the epididymal end of the vas deferens were unaffected by propylthiouracil treatment. In contrast, the potency of the β-adrenoceptor agonist, 1-isoprenaline, in inhibiting field stimulation-induced twitches of the prostatic end of the vas deferens was decreased in tissues from propylthiouracil-treated rats. Thus hypothyroidism induced by propylthiouracil produced an apparent change in the properties of postjunctional β-adrenoceptors without a concomitant reciprocal change in the properties of postjunctional α-adrenoceptors.3. Treatment of rats with propylthiouracil led to a small increase in the concentration of noradrenaline in the vas deferens, and a concomitant small increase in the rate of accumulation of 3 H-noradrenaline in in vitro experiments. Extra-neuronal uptake of 3H-isoprenaline was unaffected by propylthiouracil treatment.4. The potencies of the prejunctional α-adrenoceptor agonists, xylazine and 1-noradrenaline, in producing inhibition of twitches evoked by field stimulation of preparations of the prostatic end of the vas deferens, were similar in preparations from propylthiouracil-treated and control rats, although the slope of the log dose-response curve to xylazine was decreased in the former group. Thus unequivocal changes in the properties of prejunctional α-adrenoceptors did not accompany the other prejunctional effects of propylthiouracil upon endogenous noradrenaline levels and neuronal uptake of 3H-noradrenaline in this organ.

Notes: The aim of this article is to review the literature concerning the nature and function of the sympathetic innervation of the mammalian ovary. We focus our attention upon evidence relating to suggestions that ovarian smooth muscle participates in ovulatory events, and that such participation may be modulated by the local neural supply. Guttmacher & Guttmacher (1921) mentioned that this possibility was first suggested nearly 70 years before they observed smooth muscle-like cells in the follicular walls of sow ovaries and found that isolated follicular walls were contracted by physostigmine and relaxed by adrenaline. However, Claessen (1947), using polarisation microscopy, was unable to confirm the presence of smooth muscle in the apices of follicles from a number of species, and interest in the Guttmachers' findings temporarily lapsed.In 1967, Jacobowitz & Wallach reported the findings of a histological study of ovaries from cats, monkeys and humans in which they observed catecholamine fluorescence associated with smooth muscle-like cells in the stroma. In 1969, Rocereto, Jacobowitz & Wallach demonstrated that the cat isolated ovary exhibited spontaneous mechanical activity and was reactive to catecholamines. These investigations together with those of Owman & Sjöberg (1966) and Sjoberg (1967) initiated a resurgence of interest in the possibility that the adrenergic innervation of the ovary may play a functional role in ovarian processes; in particular that it might affect the contractility of smooth muscle and so participate in ovulation.With the development of techniques such as electron microscopy and fluorescence histochemistry, together with greater sophistication of pharmacodynamic analysis, an increasing number of publications concerned with the role of smooth muscle and adrenergic innervation in the ovary has appeared in the recent literature. Reference to some of this work is found in the reviews of Marshall (1972, 1973) and Bell (1972). A comprehensive review devoted specifically to the roles of catecholamines and nerves in ovulation was published by Bahr, Kao & Nalbandov in 1974. Their review described the sympathetic innervation of avian as well as of mammalian ovaries and the possible function of such innervation. They considered evidence relating to several possible roles, including modification of contraction of ovarian smooth muscle, participation in ovulation, and/or control of the ovarian vasculature, and concluded that nerves play some role in ovulation, but that it is not clear how this effect is mediated.

Notes: 1. Testosterone propionate (0·5 mg/day) administered for 5 weeks to prepubertal rats increased the weight of sex accessory organs but did not alter the rate of gain of body weight. Methandienone, given in a similar dosage regimen, was without effect on these parameters. The synthetic progestagen, norgestrel, administered orally in a dose of 0·5 mg/day increased the weight of the vas deferens but was without effect on seminal vesicle and testis weights and on the growth rate. Given in combination with testosterone, norgestrel caused a marked decrease in testis weight and reversed the effects of testosterone propionate on seminal vesicle weight. Thus, in the dosage regimen used, this progestagen exhibited an endocrine profile comprising androgenic, synandro-genic and anti-androgenic effects.2. Rats, which were castrated when they weighed 70–80 g, exhibited rates of gain of body weight which were similar to those of control animals. Testosterone propionate in the doses used reversed castration-induced atrophy of the vas deferens and seminal vesicle.3. The contractility of the vas deferens of intact rats, determined by direct field electrical stimulation, was unaffected by treatment with the steroids used in this study. However, there was a marked impairment of the contractility of the vas deferens following castration, which was not fully restored by testosterone propionate in the dosage regimen used.4. The efficacies and potencies of the α-adrenoceptor agonists phenylephrine and 1-metaraminol in causing contraction of the vasa deferentia from intact rats were unaffected by the steroid treatments. In contrast, these agonists did not produce sustained, dose-dependent contractions of the vasa deferentia from castrated rats; however testosterone propionate fully restored the efficacy and potency of both agonists.5. It is concluded from this study that although adequate testosterone levels are necessary for the maintenance of contractility in the rat vas deferens, the integrity of postjunctional adrenoceptors in not modified by a variety of steroid treatments.

Notes: 1. The actions of angiotensin II, bradykinin, oxytocin, arginine vasopressin, relaxin, serotonin and the prostaglandins E2 and F2α were examined on preparations of costo-uterine muscle from stilboestrol-treated rats.2. All the agonists, except relaxin, when used in concentrations which contract the rat uterus, also produced contractions of costo-uterine muscles. Concentration-response curves were steep and maximal responses to the agonists were comparable. The negative log molar EC50 values were: serotonin, 6.5; angiotensin II, 8.8; bradykinin, 8.4; PGE2, 8.3; PGF2α, 7.1. The EC50 values (units/L) for oxytocin and vasopressin were 4.4 and 2.7 respectively.3. Indomethacin (2.8 or 5 μmol/L) did not decrease the contractile effects of the peptides or serotonin. The effects of serotonin were reduced, but not reversed, by methysergide (0.94 μmol/L).4. Porcine relaxin inhibited field stimulation-induced contractions of costouterine muscle and uterine horns from immature rats pretreated with oestradiol cypionate and from stilboestrol-treated mature rats. It was much less potent, and its effects were less clearly concentration-related, on costo-uterine muscle.5. The inhibitory effects of relaxin on the uterus were unaffected by propranolol (1 μmol/L), confirming that on this tissue relaxin acts independently of the release of catecholamines. Progesterone (30 μmol/L) was also without effect on the action of relaxin on the uterus.6. These results taken together indicate that the costo-uterine muscle of the rat: (i) contracts in response to serotonin and the peptides angiotensin II, arginine vasopressin, bradykinin and oxytocin independently of the release of the contractile prostaglandins F2α and E2; and (ii) in contrast to the uterus, may lack a significant population of receptors for relaxin. These differences from the whole uterine horn of this species may reflect the absence of endometrial tissue, and/or of sensitivity of the smooth muscle cells of the costo-uterine muscle to oestrogen.

Notes: Zusammenfassung Vorläufige Untersuchungen über die Verwandlung von LSD und Ergometrin bei der Ratte zeigen, dass von beiden Substanzen zwei Hauptprodukte gewonnen werden. Beide Metaboliten von LSD antagonisieren 5-HT am isolierten Rattenuteruspräparat; es scheint sich um hydroxilierte und konjugierte Derivate des LSD zu handeln.

Notes: Abstract The effects of histamine have been studied on separated circular and longitudinal myometrial layers from the guinea-pig. Virgin guinea-pigs in dioestrus were (1) untreated, (2) treated for 14 days thrice weekly with oestradiol cypionate 20 μg/kg s.c., or (3) treated as in (2) but in addition with progesterone 3 mg/animal s.c. daily for 4 days before use. Preparations were field-stimulated (60 V 2 ms 30 Hz for 5 s every 100 s) to elicit regular contractions. Histamine was equipotent in producing enhancement of evoked contractions of circular myometrium from animals in each treatment group (pD2=5.03, 5.05 and 4.95 in groups 1, 2 & 3 respectively), and enhanced contractility in all but two longitudinal myometrial preparations. Treatment with oestradiol alone, and with oestradiol and progesterone following oestradiol priming enhanced the magnitude of maximal response and produced a small decrease in the potency of histamine on the longitudinal myometrium. pA2 estimates for mepyramine as an antagonist were similar (8.6) in preparations of longitudinal myometrium from each group of animals. Metiamide (1–10 μmol/l) did not antagonise the effects of histamine in this layer. These results, taken together, indicate that ovarian steroids act selectively on the longitudinal myometrial layer to amplify the action of histamine, but do not alter the histamine receptor subtype which in this layer is exclusively H1.