Drugs online research references
Eur J Pharmacol. 1989 Sep 13;168(2):159-67.
Effects of muscarinic receptor agonists and antagonists on alpha 2-adrenoceptors in rat brain.
Hollingsworth PJ, Smith CB.
Department of Pharmacology, University of Michigan Medical School, Ann Arbor 48109.
The specific binding of [3H]clonidine to alpha 2-adrenoceptors on neural membranes isolated from six brain areas was determined with rats treated for various periods of time with the muscarinic agonists, oxotremorine or pilocarpine, or with the muscarinic antagonists atropine, atropine methyl nitrate, scopolamine and scopolamine methyl bromide. Administration of pilocarpine, 10 mg/kg, twice daily i.p. for 1 and 14 days increased markedly the number of alpha 2-adrenoceptors on neural membranes from all six brain areas. In contrast, oxotremorine, 0.3 mg/kg, twice daily i.p., for 7 days decreased the number of alpha 2-adrenoceptors on membranes from all brain areas except the brainstem and caudate nucleus. Both atropine and scopolamine increased the density of alpha 2-adrenoceptors in specific brain areas. Neither atropine methyl nitrate nor scopolamine methyl bromide had an appreciable effect upon the specific binding of [3H]clonidine to neural membranes from most brain areas.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2558024&dopt=Abstract
Pharmacol Biochem Behav. 1986 Jul;25(1):171-9.
Effects of muscarinic receptor antagonism upon two forms of stress-induced analgesia.
Sperber ES, Kramer E, Bodnar RJ.
The present study assessed in rats the effects of muscarinic receptor antagonism upon analgesia induced by cold-water swims (CWS: 2 degrees C for 3.5 min) and 2-deoxy-D-glucose (2DG: 600 mg/kg). First, CWS analgesia was significantly reduced 30 min after the swim by scopolamine (0.01 and 0.1 mg/kg) and methylscopolamine (10 mg/kg) pretreatment, and was eliminated 60 min after the swim by scopolamine (0.01-10 mg/kg) and methylscopolamine (1,10 mg/kg) pretreatment. In contrast, scopolamine potentiated CWS hypothermia. Second, while scopolamine (1 mg/kg) and methylscopolamine (1,10 mg/kg) pretreatment prolonged 2DG analgesia, both antagonists dose-dependently reduced 2DG hyperphagia. Third, the changes in analgesic and hypothermic stress responses were not due to baseline shifts in jump thresholds or body temperatures. However the dose-dependent reductions by scopolamine and methylscopolamine in baseline food intake and 2DG hyperphagia were significantly correlated. Fourth, the dose-dependent reduction by scopolamine and methylscopolamine of pilocarpine analgesia differed in pattern from the other analgesic effects, suggesting heterogeneity in muscarinic receptor modulation of different analgesic responses.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3749224&dopt=Abstract
Acta Physiol Scand. 1993 Mar;147(3):289-95.
Studies of muscarinic receptor reserve linked to phosphoinositide hydrolysis in parotid gland and cerebral cortex.
Ek B, Antonsson BM.
Department of Physiology, University of Gothenburg, Sweden.
Hydrolysis of inositol phospholipids caused by muscarinic agonists was studied in the guinea-pig parotid gland (PG) and cerebral cortex (CX). The present study describes the effect of two muscarinic agonists, carbachol and oxotremorine, on stimulation of phosphoinositide hydrolysis and on binding of [3H]NMS in the presence of the irreversible muscarinic antagonist benzilyl choline mustard (BCM). Carbachol and oxotremorine stimulated the formation of inositol phosphates in PG, pD2(Carb) = 5.3 +/- 0.1, pD2(Oxo) = 5.9 +/- 0.1 and in CX, pD2(Carb) = 4.3 +/- 0.2, pD2(Oxo) = 5.8 +/- 0.2. In the present study slices from both tissues have been exposed to 0.1 microM BCM for 2, 5 and 10 min. Treatment for 10 min caused a 75-85% reduction in specific [3H]N-methyl scopolamine ([3H]NMS) binding sites in both PG and CX. Following 2 min BCM treatment of PG a marked decrease in pD2 value of the carbachol-stimulated inositol phosphate formation was found. This effect was not found in CX. The results showed that a 30-40% reduction in binding sites shifted the carbachol concentration response curve to the right by one order of magnitude and reduced the oxotremorine-induced release of inositol phosphates by approximately 20%. In PG, the BCM-induced reduction of the carbachol-stimulated inositol phosphate formation was paralleled by the reduction in receptor binding sites. Similar treatment, but in CX, showed a lower reduction of the carbachol-stimulated inositol phosphate formation as compared to the reduction in receptor-binding sites.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8386426&dopt=Abstract
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