Drugs online research references
Arch Int Pharmacodyn Ther. 1989 Nov-Dec;302:96-106.
Interactions of carteolol and other beta-adrenoceptor blocking agents with serotonin receptor subtypes.
Nishio H, Nagakura Y, Segawa T.
Department of Pharmacology, Hiroshima University School of Medicine, Japan.
The importance of the anti-serotonergic activity of carteolol and other beta-adrenoceptor blockers in their efficacy as anti-migraine agents has been examined in the membrane fraction of rat brain frontal cortex and pig choroid plexus, using radioligand binding methods. Carteolol and l-propranolol, which are suggested to have anti-migraine activity in man, were found to be active inhibitors of the binding of [125I]ICYP to 5-HT1B recognition sites and of [3H]-8-OH-DPAT to 5-HT1A recognition sites. Carteolol is devoid of activity at 5-HT1C and 5-HT2 recognition sites, whereas l-propranolol shows substantial affinity for these receptor subtypes. Atenolol, another beta-adrenoceptor blocker with anti-migraine activity, is devoid of activity at any of the 5-HT receptor subtypes examined. The possibility that carteolol and other beta-adrenoceptor antagonists exert their pharmacological effects through central 5-HT receptor subtypes is discussed in relation to the potential mechanism of the anti-migraine activity of carteolol.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2576893&dopt=Abstract
Cytobios. 1989;58(234-35):171-7.
Selective sensitive period in chick embryo: toxic effect of exogenous neurotransmitters.
Zamenhof S.
Department of Microbiology and Immunology, UCLA School of Medicine 90024-1747.
The phenomenon of sudden mortality in the chick embryo, induced by the exogenous neurotransmitters norepinephrine, epinephrine, dopamine, serotonin, carbachol, and by the beta-blockers propranolol and atenolol, is described. When introduced singly into eggs (albumen) in doses of 0.1 mg per egg, these substances induced highly significant, sharply increased mortality (60% to 100%) when the introduction was on embryonic (incubation) days 8 to 12 (hereafter called E8 and E12), but none if introduction was earlier. These ages follow the appearance of functional receptors (or receptor-effectors) for these substances. However, the involvement of receptors here has not been proved. Solvent alone (Ringer's solution for chick) had no effect, indicating that the procedures used were in themselves not lethal. Possibly, the above neurotransmitters became lethal to the embryo because they were introduced in excess of the amounts which were produced and needed at that time by the embryo for optimal development.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2574100&dopt=Abstract
Br J Pharmacol. 1986 Jan;87(1):265-77.
The role of catecholamines in the production of ischaemia-induced ventricular arrhythmias in the rat in vivo and in vitro.
Daugherty A, Frayn KN, Redfern WS, Woodward B.
The role of catecholamines in the production of ischaemia-induced ventricular arrhythmias in vivo and in vitro was studied using coronary artery ligation in the rat. Increases in plasma catecholamine concentrations during coronary artery ligation in pentobarbitone-anaesthetized animals were prevented by either acute adrenalectomy or chronic adrenal demedullation, but these procedures did not protect against the occurrence of ventricular arrhythmias. Thus plasma catecholamines were not obligatory mediators of arrhythmogenesis. Three protocols were used in vitro to evaluate the possible influence of intramyocardial release of noradrenaline, produced by the local conditions of ischaemia, on the production of ventricular arrhythmias. During coronary artery ligation in isolated perfused hearts, no enhanced output of 3H could be detected from [3H]-noradrenaline loaded hearts, even in the presence of inhibitors of catecholamine uptake processes, although washout of lactate from ischaemic regions was readily demonstrable. Both optical isomers of propranolol were equally effective in reducing the incidence of arrhythmias, implying a non-specific effect, since the (+)-isomer possesses considerably less beta-adrenoceptor blocking activity. The equipotency of optical isomers of propranolol combined with a lack of effect of atenolol suggested that arrhythmia production was not a consequence of beta-adrenoceptor stimulation. The alpha-adrenoceptor blockers phentolamine and prazosin, both exerted antiarrhythmic actions of similar potency, but phenoxybenzamine and trimazosin had no significant effects. An evaluation of the pharmacological properties of the alpha-adrenoceptor blockers showed that those drugs which had demonstrable local anaesthetic properties also exerted significant antiarrhythmic effects. No relationship was found between potency of alpha-adrenoceptor blockade and antiarrhythmic efficacy. The overall conclusion from these multifaceted approaches was that catecholamines were not necessary mediators of the early phase of ventricular arrhythmias in the rat.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2869812&dopt=Abstract
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