Drugs online research references
Comp Biochem Physiol C. 1993 Feb;104(2):327-32.
Pharmacological evidence for the presence of a beta-adrenoceptor-like agonist in the amphinoid polychaete Eurythoe complanata.
Suadicani SO, de Freitas JC, Sawaya MI.
Departamento de Fisiologia Geral, Instituto de Biociencias, Universidade de Sao Paulo, Brazil.
1. Methanolic extracts from the body wall of Eurythoe complanata (ExEc) were tested for biological activity on the isolated rat ileum. 2. ExEc produced either relaxation or relaxation followed by contraction of the rat ileum in a concentration-dependent manner. 3. The predominant relaxation response to ExEc was completely blocked by the beta-adrenoceptor antagonist propranolol and was unaffected by the alpha-adrenoceptor antagonist phenoxybenzamine. 4. The results indicate that the relaxation induced by ExEc is mediated by beta-adrenoceptors. The presence of a myorelaxing substance in E. complanata that selectively activates the beta-adrenoceptors is suggested.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8098686&dopt=Abstract
Pharmacol Biochem Behav. 1993 May;45(1):209-14.
Cocaine-induced elevation of plasma corticosterone is mediated by different neurotransmitter systems in rats.
Sarnyai Z, Biro E, Telegdy G.
Institute of Pathophysiology, Albert Szent Gyorgyi Medical University, Szeged, Hungary.
It has previously been demonstrated that cocaine stimulates the hypothalamic-pituitary-adrenal (HPA) axis through hypothalamic corticotropin-releasing factor (CRF) secretion. The role of different neurotransmitters in mediation of the cocaine-induced elevation of plasma corticosterone (CORT) were investigated in rats by using transmitter antagonists. Peripheral (IP) pretreatment with a dopaminergic antagonist, pimozide (0.01-1.0 mg/kg, IP), a noradrenergic blocker, phenoxybenzamine (1.0-4.0 mg/kg, IP), a beta-adrenergic blocker, propranolol (0.2-10 mg/kg, IP), an opiate antagonist, naloxone (1.0-4.0 mg/kg, IP), and a muscarinic cholinergic antagonist, atropine (1.0-4.0 mg/kg, IP), inhibited the cocaine-induced CORT response dose dependently. A similar dose-dependent inhibition of the plasma CORT response induced by cocaine was observed after the ICV route of administration of these antagonists in microgram quantities. None of the investigated IP or ICV doses of transmitter antagonists altered the basal CORT level. These results suggest that the activation of multiple neurotransmitter systems, including catecholaminergic, opiate, and cholinergic systems, might be responsible for the cocaine-induced HPA axis activation, probably through the specific receptors located in the CNS.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8100073&dopt=Abstract
Biochem Pharmacol. 1993 Jul 6;46(1):125-30.
Endogenous factor activating Na,K-ATPase induced by blockade of adrenoceptors.
Manukhin BN, Erokhov PA, Volina EV.
Institute of Developmental Biology, Russian Academy of Sciences, Moscow.
It was established that the regulatory factor released from the effector cells under the blockade of postsynaptic alpha- and beta-adrenoceptors by phentolamine and propranolol (0.5-1.0 microM) and activating noradrenergic uptake and synthesis increased the activity of Na,K-ATPase of isolated rat organs and partially purified Na,K-ATPase isolated from the rat brain. The regulatory factor is a protein with molecular mass 25-100 kDa, adsorbed on phenylsepharose CL-4B and eluated with 30 mM KCl. It consists of two active components with pI 5.1 and 5.9 which in admixture (1:1) activate Na,K-ATPase by 60%.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8102232&dopt=Abstract
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