Anterior Pituitary

Daughaday, William H.

doi:10.1007/978-1-4684-2502-4_2

Cited by 10 publications

(15 citation statements)

References 127 publications

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“…Nonetheless, these animals are not obese relative to older animals (Mueller and Hsiao, 1980). Since growth hormone, which shows high levels at this time (Eden, Albertsson-Wikland, and Isaksson, 1978;Dickerman, Dickerman and Meites, 1972;Ojeda and Jameson, 1977), stimulates rapid growth of lean body mass and inhibits lipogenesis (Daughaday, 1979), one would expect little accummulation of body fat in prepubertal females. Based on these data, one might hypothesize that changes in body weight following estrogen treatment might not specifically affect adiposity since fat content is already low.…”

Section: Peripheral Sites Of Hormone Actionmentioning

confidence: 99%

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Effects of estradiol and progesterone on food intake, body weight, and carcass adiposity in weanling rats

Schwartz¹,

Wade²

1981

American Journal of Physiology-Endocrinology and Metabolism

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Section: Peripheral Sites Of Hormone Actionmentioning

confidence: 99%

“…Effects of GH on bone and cartilage are mediated primarily through the action of somatomedins, growthpromoting peptides (Daughaday, 1979;Martin, 1976). Thus, estrogens might alter skeletal growth by inhibiting somatomedin synthesis.…”

mentioning

confidence: 99%

Effects of estradiol and progesterone on food intake, body weight, and carcass adiposity in weanling rats

Schwartz¹,

Wade²

1981

American Journal of Physiology-Endocrinology and Metabolism

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“…The attempt to follow the time course of CO-hemoglobin formation failed in glucose treated mice due to a difficulty in blood sampling which was caused by a high in crease in blood viscosity. On the other hand, a possibility that glucose-induced hyper glycemia increases secretion of various hor mones including insulin which then could protect mice from asphyxia led us to test the effect of L-arginine, a strong stimulant of insulin and growth hormone secretion (13). The amino acid was found to be active both orally and intraperitoneally, but the effective dose by the former route was higher than the one by the latter route, indicating that the El axis (14) would not practically contribute to the action of the amino acid given orally.…”

Section: Discussionmentioning

confidence: 99%

Carbon monoxide (CO)-induced hypoxia in mice: Evaluation as an experimental model of cerebral ischemia for drug screening.

Koida¹,

Nakamuta²,

Yasuda³

et al. 1989

Jpn.J.Pharmacol

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Abstract-An injection of 12.5 ml of carbon monoxide (CO) gas into an air-filled chamber (780 ml in volume) caused the death of the ICR or ddY mouse (6-8 weeks old) inside. The average survival time was 2.5 min for either sex of animals treated with nothing or saline and never exceeded 8 min. Pretreatment with pentobarbital Na (30 mg/kg, i.p.), hopantenate Ca (100 mg/kg, i.p.), vinpocetine (5 mg/kg, i.p. or 50 mg/kg, p.o.), flunarizine HCI (5 mg/kg, i.p.), glucose (6 g/kg, i.p.), pheno barbital (30 mg/kg, i.p.), phenytoin (20 mg/kg, i.p.), arginine HCI (100 mg/kg, i.p. or 1 g/kg, p.o.) and alanine (100 mg/kg, i.p. or 1 g/kg, p.o.) prolonged the survival time of male mice. Insofar as tested, female mice responded rather poorly to these pretreatments. Survival for longer than 8 min occurred in some of the drug-pretreated animals of either sex. To be noted is the finding that most of the animals which survived 8 min once were able to survive the second 8 min on the following day without any drug-treatment.Monitoring of the time course of carboxyhemoglobin formation revealed that the carboxyhemoglobin level reached a plateau of 70% saturation within 2 min and then gradually increased. The lethal level was about 72%. Pentobarbital decreased the formation rate but did not elevate the lethal level. The results indicate that the CO-induced hypoxia model of mice is usable for screening of drug candidates which may be effective for treatment of human ischemic diseases.

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“…PRFs, on the other hand, are important in mediating the rise in prolactin release under a variety of physiological and experimental conditions. A number of hypothalamic stimulating factors such as thyrotropin-releasing hormone (TRH), cholecystokinin, vasoactive intestinal polypeptide (VIP), and neurotensin have been identified, but their role in the physiological regulation of prolactin secretion is not yet certain (11). Under several of the stimulatory conditions studied, for example during suckling, the level of DA in portal blood decreases, and there has been a suggestion that the fall of DA in portal blood, although very transient, is a pre-requisite for a full prolactin response to PRF (2,12).…”

Section: Introductionmentioning

confidence: 99%

Dopamine agonists both stimulate and inhibit prolactin release in GH4ZR7 cells

Chang

1999

European Journal of Endocrinology

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Prolactin secretion from the anterior pituitary gland is regulated by multiple factors including prolactin-release inhibiting factors (PIFs) and prolactin releasing factors. PIFs, however, usually dominate to exert a tonic inhibition in the biological system, and the physiological PIF is believed to be dopamine. However, there is accumulating evidence that dopamine can not only inhibit but also stimulate prolactin release. Many investigators believe that this is achieved by activating inhibitory and stimulatory subtypes of dopamine receptors. We tried to demonstrate that one subtype of dopamine receptors is capable of both inhibiting or stimulating prolactin release using GH 4 ZR 7 cells. GH 4 ZR 7 cells express only a short form of dopamine D 2 receptors (D 2s ). Low concentrations of three well-established D 2 receptor agonists (dopamine, apomorphine and bromocriptine) stimulated prolactin release from GH 4 ZR 7 cells while high concentrations inhibited the release. Haloperidol, a D 2 receptor antagonist, blocked the inhibitory action, but was unable to block the dopamine-induced stimulatory action. Pretreatment of cells with phenoxybenzamine, a receptor alkylating agent, abolished both the dopamine-induced stimulatory and inhibitory actions. Our results support the thesis that the stimulation of prolactin release induced by dopamine is mediated through dopamine D 2s receptors since the GH 4 ZR 7 cells have only D 2s receptors among dopamine receptors. We have concluded that the D 2s receptor is capable of both stimulating and inhibiting prolactin release, probably via the activation of a G s protein by low concentrations and a G i protein by high concentrations of dopaminergic agents.

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Anterior Pituitary

Cited by 10 publications

References 127 publications

Effects of estradiol and progesterone on food intake, body weight, and carcass adiposity in weanling rats

Effects of estradiol and progesterone on food intake, body weight, and carcass adiposity in weanling rats

Carbon monoxide (CO)-induced hypoxia in mice: Evaluation as an experimental model of cerebral ischemia for drug screening.

Dopamine agonists both stimulate and inhibit prolactin release in GH4ZR7 cells

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