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Biomedical subjects

P Leroux

Publications and source records attributed to P Leroux.

At least 91 records · Page 5Linked to original sources
PubMed1983

Effect of Tyr-Pro-Leu-Gly-NH2 on melanotropin-stimulating hormone release in the frog and rat.

The tetrapeptide Tyr-Pro-Leu-Gly-NH2 (Tyr-MIFI) has been recently characterized in the hypothalamus and pineal of the rat. Since the concentration of Tyr-MIFI in the brain is increased by pinealectomy and is higher when the animals are in the dark, the possibility that Tyr-MIFI could be a physiological regulator of melanotropin secretion has been investigated. For this study a well-defined perifusion model has been applied, using whole neurointermediate lobes from male frogs (Rana ridibunda Pallas) or male Wistar rats. The amount of alpha-MSH released in the effluent perifusate was measured by means of a sensitive and specific radioimmunoassay method. For concentrations ranging from 10(-10) to 10(-6) M, Tyr-MIFI did not significantly alter the spontaneous release of alpha-MSH in the frog nor did it alter the release of alpha-MSH in the rat. Since it has been recently demonstrated that the tripeptide pGlu-His-Pro-NH2 (mammalian TRH) is a specific MSH-releasing factor in the frog, the possibility that Tyr-MIFI could modulate the response of the intermediate lobe of the frog to TRH has also been investigated. No alteration of TRH-induced alpha-MSH release was observed in the presence of a 100-fold excess of Tyr-MIFI. In addition, Tyr-MIFI was found to be unable to lighten the skin of the frog (Rana pipiens) when applied directly to the pituitary of the darkened animals. Thus these results definitively rule out the possibility that Tyr-MIFI is the melanotropin-release inhibiting factor in the frog or rat.

Animals↗
PubMed1983

Catecholaminergic control of alpha-melanocyte-stimulating hormone (alpha MSH) release by frog neurointermediate lobe in vitro: evidence for direct stimulation of alpha MSH release by thyrotropin-releasing hormone.

The role of dopaminergic and adrenergic innervation of the intermediate lobe of amphibian pituitary in the release of alpha MSH has been studied in vitro. Neurointermediate lobes of frog (Rana ridibunda Pallas) have been perifused in amphibian culture medium (ACM) for 5-7 h. alpha MSH released in the effluent perifusate was measured by means of a sensitive and specific RIA. No significant morphological alteration of neurointermediate lobe cells was observed during the perifusion experiment, even at the electron microscopic level. The existence of dopaminergic receptors, responsible for an inhibition of frog melanotrophs, was shown using the dopaminergic agonists apomorphine (10(-6) M) and bromo-2-ergocryptine (10(-8) and 10(-7) M), which initiated a marked reduction of alpha MSH secretion. The effect of apomorphine was obliterated by the dopaminergic antagonist haloperidol. Haloperidol itself induced a dose-related stimulation, and the monoamine oxidase inhibitor nialamide (4 x 10(-3) M) inhibited alpha MSH secretion. In addition, haloperidol led to a complete reversal of the inhibitory effect of nialamide on alpha MSH secretion. These results demonstrate the existence, in the parenchyme of the intermediate lobe, of dopaminergic nerve fibers that are functionally active. The beta-adrenergic agonist isoproterenol was responsible for a dose-related stimulation of alpha MSH secretion; the stimulatory effect was reversed by the beta-adrenergic antagonist propranolol. TRH is a potent stimulator of alpha MSH secretion in amphibians. Since haloperidol and propranolol did not abolish the stimulation of alpha MSH release induced by TRH, it appeared that TRH action was not mediated via an inhibition of dopamine release or via a stimulation of adrenergic nerve fibers.

Animals↗
PubMed1983

Effect of ranitidine on healing of peptic ulcer: a 2-month study.

A multicenter trial of oral ranitidine 150 mg bid was conducted in 41 patients with duodenal and 30 with gastric ulcers. Patients were randomly allocated in double-blind fashion to 4 wk treatment with either ranitidine or placebo, after which all unhealed patients were given 4 wk on the active drug without breaking the original allocation code. After 4 wk of treatment the healing rate associated with ranitidine was significantly superior to that of placebo in both duodenal and gastric ulcer patients. Further improvement in cumulative healing rates was observed after the 2nd month of the study. After the allocation code was broken and all patients had had the opportunity of up to 8 wk on the active drug, there remained only a single unhealed pyloric ulcer. No serious adverse effects or biochemical abnormalities were observed. Ranitidine is a potent and well-tolerated H2 antagonist. Therapy for 4 or 8 wk is highly effective in the treatment of uncomplicated gastroduodenal ulcer.

Adult↗
PubMed1982

Effect of aldosterone antagonists on mineralocorticoid synthesis in vitro. Inhibition of aldosterone production by prorenoate-K.

A perifusion technique using frog adrenal glands has been applied to investigate the effects of long-term administration of a new aldosterone antagonist (potassium prorenoate; SC 23992) on mineralocorticoid production. Whatever the duration of administration of potassium prorenoate, at a constant concentration of 5 X 10(-4) M, a significant inhibition of aldosterone output occurred during the passage of the compound. The inhibition was immediate (lag period less than 10 min); the amplitude of the inhibition was constant during the whole experiment and ranged from 77 to 89%; the aldosterone output returned to a regular basal value 80-100 min after the end of infusion of potassium prorenoate. We have also investigated the effect of a concentration gradient of potassium prorenoate (similar to the concentration gradient of aldosterone antagonist observed in plasma after a single oral administration of the molecule) upon aldosterone production over 12 h. From this study, we have established the existence of a highly significant correlation between the extent of the inhibition of aldosterone production and the concentration of the aldosterone antagonist. Finally we have observed that potassium prorenoate blocked the stimulation of aldosterone secretion induced by synthetic ACTH and significantly reduced the angiotensin-induced aldosterone stimulation. The present results indicate that, besides the well-known competitive inhibition of aldosterone binding exerted by potassium prorenoate at the renal receptor site, a direct inhibition of aldosterone biosynthesis also accounts for the pharmacological activity of this aldosterone antagonist.

Adrenocorticotropic Hormone↗
PubMed1981

Effect of hypophysectomy and pituitary stalk transection on alpha-melanocyte-stimulating hormone-like immunoreactivity in the brain of the frog, Rana ridibunda Pallas.

The existence of an alpha-MSH-like molecule in the frog brain led us to investigate the role of the pituitary gland in the maintenance of the alpha-MSH content in 3 different regions of the brain. Acetic acid extracts of hypothalamus, rhombencephalon and telencephalon were analyzed by means of a highly specific radioimmunoassay for alpha-MSH in normal, sham-operated, pituitary disconnected and hypophysectomized frogs. Transection of the pituitary stalk gave rise to a significant decrease in alpha-MSH content in the intermediate lobe of the pituitary gland (-71% after 3 days), but did not affect alpha-MSH content in the distal lobe or in the brain. Eight days after total hypophysectomy, an alpha-MSH immunoreactive compound, co-eluting with synthetic alpha-MSH on Sephadex G-25, was found in the 3 brain regions studied. Removal of the whole pituitary gland did not significantly modify alpha-MSH content in the hypothalamus and the telencephalon. A slight increase in alpha-MSH was even observed in the rhombencephalon of hypophysectomized animals. Furthermore, no modification in alpha-MSH immunoreactivity occurred in any region of hypophysectomized animals. These results demonstrate the existence of alpha-MSH-like material in the brain of Rana ridibunda and establish that brain alpha-MSH in the frog is not of pituitary origin.

Animals↗
PubMed1981

Stimulatory effect of prostaglandin E1 on thyroliberin-induced alpha-melanotropin release from perifused neuro-intermediate lobes of frog pituitary gland.

A possible direct effect of prostaglandins on alpha-melanotropin (alpha-MSH) release at the level of the intermediate lobe of the frog pituitary was investigated in vitro using a perifusion system technique. The effect of prostaglandins was studied on both spontaneous and TRH-stimulated alpha-MSH secretion. No significant effect of PGE1, PGE2, PGF1 alpha or PGF2 alpha on basal release of alpha-MSH could be detected. Indomethacin did not alter the alpha-MSH release induced by TRH. Conversely a significant increase in TRH-induced alpha-MSH secretion was observed in the presence of 1 x 10(-6) M PGE1. This magnifying effect was directly related to the concentration of TRH for doses ranging from 1 x 10(-8) M to 1 x 10(-6) M.

Animals↗
PubMed1980

[Development of the mono-oxygenase system. Implications in perinatal pharmacotoxicology (author's transl)].

The hepatic or extra-hepatic mono-oxygenase activities ensure the metabolism of exogenic hydrophobic substances (xenobiotics) and endogenic substances (steroids). These substances easily cross the placenta ; it is of primary importance to know perfectly their possible transformation at the level of the foetus together with their excretion from the foetal compartment. We summarise here the data in the literature which describe the development of the mono-oxygenase system and the microsomal enzyme activities of phase II (epoxide hydrolase and UDP-glucuronosyl-transferase) both in the laboratory animal and in the human foetus. The influence of various factors (exogenic inducers, endogenic hormones) on the development of these activities is also reported. Although a conclusion is difficult concerning the present state of our knowledge, the main pharmacotoxicological consequences of the development of mono-oxygenasic activities are considered.

Adrenal Cortex Hormones↗