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851.
852.
A.M. Attia B.A. Richardson C. Rodriguez M.H. Mostafa S.A. Soliman A.H. El-Sebae R.J. Reiter 《Brain research》1991,554(1-2):253-256
Lindane, a chlorinated hydrocarbon pesticide, was previously shown to enhance the nighttime rise in pineal N-acetyltransferase (NAT) activity and melatonin as well as serum melatonin levels. The purpose of the present study was to test whether lindane acts on the pineal gland by means of a beta-adrenergic receptor mechanism. Whereas lindane (total dose 17.8 mg/kg b.wt. over 6 days) by itself significantly augmented the nocturnal levels of pineal NAT activity in otherwise untreated rats, the pesticide was ineffective in reference to this enzyme when it was given in conjunction with the beta-adrenergic receptor antagonist propranolol (20 mg/kg b.wt., one hour before lights off). The augmentation of NAT activity by lindane also caused significant reductions in pineal serotonin (5-HT) and 5-hydroxyindole acetic acid (5-HIAA); again, both these responses were blocked by propranolol treatment. Neither pineal 5-hydroxytryptophan nor pineal or serum melatonin levels were significantly changed as a result of either lindane or propranolol treatment. The results are consistent with the idea that lindane influences pineal 5-HT metabolism either at the level of the beta-adrenergic receptor or via the sympathetic innervation to the pineal gland. 相似文献
853.
854.
The effects of bupropion on core body temperature of intact or reserpinized mice were studied. Intraperitoneal (IP) administration
of bupropion to mice induced a dose-dependent hypothermia. The response of bupropion was decreased by the D-2 antagonist sulpiride
or pimozide, but not by the D-1 antagonist SCH 23390, antimuscarinic drug atropine, α-adrenergic blocker phenoxybenzimine,
β-adrenergic antagonist propranolol or antiserotonergic methergoline. Reserpine induced hypothermia, which was reversed by
bupropion administration. The reversal response of bupropion was reduced by propranolol, but not sulpiride, SCH 23390, phenoxybenzamine,
atropine or methergoline. It is concluded that bupropion-induced hypothermia may be mediated through D-2 receptor activation,
while the reversal of reserpine-induced hypothermia by bupropion may be exerted through β-adrenergic stimulation. 相似文献
855.
N Cagin E Freeman J C Somberg H Bounous T Mittag R Diaz B Levitt 《European journal of pharmacology》1973,24(2):256-261
The action of propranolol on cardiotoxicity produced by ouabain was studied in intact and isolated guinea pig hearts. The lethal event in the intact guinea pig was ventricular fibrillation; in the isolated heart it was asystole. Myocardial ouabain content at death was significantly higher in isolated preparations than in the intact heart. Propranolol was observed to alter the mode of death in the intact guinea pig from ventricular fibrillation to asystole. The myocardial ouabain content at the time of death was elevated in guinea pigs pretreated with propranolol to the level observed in isolated guinea pig heart preparations. Exposure of the isolated preparation to propranolol prolonged the time to the induction of cardiac rhythm disorders and death without changing myocardial ouabain content. These data suggest that propranolol, by eliminating neural influence transforms the cardiotoxicity of ouabain to an in vitro mechanism. In the isolated heart, propranolol prolongs the time to the induction of cardiac rhythm disorders by inhibiting the myocardial uptake of ouabain. 相似文献
856.
Pretreatment with propranolol HCI resulted in a substantial reduction in the amount of 14C-morphine found in blood plasma, neostriatum plus adjacent tissue, pons-medulla, midbrain, cerebral cortex and cerebellum 25 min after IP injection of the labelled morphine. Previous observations, demonstrating attenuation of behavioral effects of morphine following pretreatment with propranolol, might have been due to a decrease in peripheral and/or central levels of morphine. However, when morphine HCI (10-20 MUM) was administered via intraventricular cannulae following pretreatment with propranolol given intraperitoneally in rats performing free operant (sidman) avoidance, the anti-avoidance effects of the opiate were also attenuated. Hence, previous results cannot be attributed solely to reduced concentration of morphine at CNS site(s) of action. 相似文献
857.
Intrarenal perfusion of dopamine (6 mug/kg/min for 10 min) caused a significant increase of renin secretion, together with a significant increase in renal blood flow. This renin hypersecretion is not accompanied by any significant alteration in renal perfusion pressure, kalemia or natriuresis. The role of intrarenal dopaminergic receptors has been studied: (a) Haloperidol (intrarenal perfusion of 50 mug/kg/min for 20 min) suppresses the renal vasodilation and renin hypersecretion induced by dopamine. (b) Propranolol (intrarenal perfusion of 1 mg/kg in 15 min, then of 4 mg/kg/hr) alters neither the renal vasodilation nor the renin hypersecretion induced by dopamine. These observations support the assumption that the dopaminergic receptors are brought into play in the two renal responses to dopamine studied by us. 相似文献
858.
Propanidid (Epontol), a general anaesthetic agent with a particularly short action in vivo significantly depressed the contraction amplitude of guinea pig isolated atria. A steep concentration-response curve could be established. Contractile force of electrically driven atria (180/min) was reduced by approximately 50% at a propanidid concentration of 3.5 x 10-4 M in the medium. The negative inotropic effect developed rapidly (less than 10 min). At concentrations of 4.5 x 10-4 M and less propanidid hardly reduced the frequency of spontaneously beating atria. The uptake of extracellular 45 Ca by spontaneously beating atria occurred significantly more slowly in presence of propanidid (4.5 x 10-4 M ), whereas the exchangeable calcium fraction remained unchanged. Accordingly, propanidid reduced the rate of exchange of calcium so that less ionized calcium was available for excitation-contraction coupling. Propanidid (4.5 x 10-4 M) accelerated the uptake of 45Ca by isolated plasma membranes, obtained from guinea pig ventricular muscle. Moreover, the binding capacity for calcium by isolated membranes was increased in presence of propanidid. These observations imply that less ionized calcium is available for activation of the contractile system. It is concluded that the negative inotropic action of propanidid is probably due to the drug's influence on membrane function, thus bringing about an important change in cellular calcium metabolism. 相似文献
859.
Antonio Mundo Salvador 《European journal of pharmacology》1975,31(1):38-43
The influence of amantadine on the contractile responses of the rat uterus to oxytocin in the presence of several ionic modifications of the external medium was studied both in situ and in vivo.Oxytocic effects of amantadine were observed in vivo (1 and 5 mg/kg), and in vitro (9.3 × 10?7 M to 2.8 × 10?6 M); possible competitive partial potentiation of the contractile effect of oxytocin was also observed.Amantadine, 9.35 × 10?6, 1.3 × 10?5 and 1.8 × 10?5 M, significantly reduced oxytocic activity.Calcium ions antagonized the oxytocic and antioxytocic effects of amantadine. Excess K+ and the presence of Mg2+ ions (1.8 mM/l and 1.08 mM/l respectively) reversed the antioxytocic effect of amantadine. Propranolol also reversed the antioxytocic effect of amantadine.It is postulated that the oxytocic effect of amantadine may be related to antagonism of calcium; antioxytocic activity may be explained by stabilization of the resting cell membrane, inhibiting ionic flow, and also by its catecholamine-liberating activity. 相似文献
860.
Summary The possibility of a protective effect by reserpine or propranolol on anoxia-induced release of malate and lactate dehydrogenase was investigated in isolated perfused hearts of guinea-pigs. After allowing 30 min of aerobic perfusion for the development of a steady state, the hearts from the nontreated group as well as the reserpine-pretreated or propranolol-treated group were subjected to a prolonged anoxia of 5 hrs. A marked enzyme release which occurred from the anoxic nontreated hearts was significantly inhibited by reserpine or propranolol. These findings suggest that the enzyme release from the anoxic myocardium is partly related to the liberation of endogenous catecholamines. 相似文献