Drugs online research references
Clin Exp Pharmacol Physiol. 1993 Feb;20(2):127-34.
Alpha- and beta-adrenoceptor agonist activity in the venom of the Australian huntsman spiders, Delena cancerides and Isopeda montana.
Korszniak NV, Story DF.
Department of Pharmacology, University of Melbourne, Parkville, Victoria, Australia.
1. Crude venom gland extracts (VGE) were prepared from female Delena cancerides and Isopeda montana spiders. The VGE were tested in isolated rat atrial, caudal artery and pithed rat preparations for pharmacological activity. 2. In rat isolated atrial preparations, D. cancerides and I. montana VGE, each in a concentration of 2 glands/mL, produced increases in atrial rate which were abolished by propranolol (1 mumol/L) but not by ketanserin (0.1 mumol/L) or reserpine pretreatment (2.5 mg/kg s.c. 24 h prior to experimentation) indicating a direct action on atrial beta-adrenoceptors. 3. In rat caudal artery preparations each VGE produced an increase in perfusion pressure, which was taken as an index of vasoconstriction. Pressor responses to D. cancerides VGE (1 gland/mL) were abolished in the presence of prazosin (1 mol/L) but not by reserpine pretreatment, indicating an action of the VGE on vascular alpha 1-adrenoceptors. Neither prazosin nor reserpine pretreatment had any effect on pressor responses of rat caudal artery preparations to I. montana VGE. Ketanserin (6 nmol/L) produced a small reduction in the degree of vasoconstriction produced by the VGE. This demonstrates a lack of alpha 1-adrenoceptor agonist activity of the VGE. 4. Both VGE produced dose-dependent increases in mean arterial pressure and heart rate in pithed rat preparations. The use of relatively selective receptor antagonists indicated that the increases in mean arterial pressure (MAP) produced by both VGE were mediated by an action on alpha 2-adrenoceptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8095195&dopt=Abstract
Acta Med Okayama. 1993 Feb;47(1):29-33.
Nipradilol depresses cardiac contractility and O2 consumption without decreasing coronary resistance in dogs.
Zhao DD, Namba T, Araki J, Ishioka K, Takaki M, Suga H.
Second Department of Physiology, Okayama University Medical School, Japan.
Nipradilol (3,4-dihydro-8-(2-hydroxy-3-isopropylamino) propoxy-3-nitroxy-2H-1-benzopyran) is a newly synthesized chemical agent designed to possess beta-adrenoceptor blocking and vasodilating actions. Nipradilol decreased left ventricular contractility index (Emax, slope of the ventricular end-systolic pressure-volume relation), systolic pressure-volume area (PVA, a measure of ventricular total mechanical energy) and oxygen consumption in cross-circulated excised dog hearts. However, nipradilol did not decrease total coronary resistance. These results indicate that nipradilol, like propranolol, depresses myocardial mechanoenergetics and that the vasodilating action of nipradilol could not be detected in the present study.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8096354&dopt=Abstract
Am J Physiol. 1993 Mar;264(3 Pt 1):E403-12.
Coexistence of beta 1-, beta 2-, and beta 3-adrenoceptors in dog fat cells and their differential activation by catecholamines.
Galitzky J, Reverte M, Portillo M, Carpene C, Lafontan M, Berlan M.
Institut National de la Sante et de la Recherche Medicale, Faculte de Medecine, Universite Paul Sabatier, Toulouse, France.
The existence of a beta 3-adrenoceptor (in addition to classical beta 1- and beta 2-), its involvement in the control of lipolysis and its recruitment by catecholamines were investigated in dog adipose tissue. Isoproterenol, norepinephrine, and the beta 2-selective agonist procaterol fully activated lipolysis in adipocytes (order of potency: isoproterenol > norepinephrine = procaterol). beta 3-Adrenergic agonists stimulated lipolysis with the order of potency: BRL 37344 > CGP 12177 > SR 58611A. Propranolol and bupranolol (nonselective beta-antagonists) antagonized, with a low potency, the effect of BRL 37344, whereas the beta 1-antagonist CGP 20712A and the beta 2-antagonist ICI 118551 were without action. CGP 20712A inhibited the effect of lower concentrations of agonists (0.05 microM isoproterenol, 0.1 microM norepinephrine and 0.1 microM procaterol) with an inhibitory constant (mean Ki) of 0.0075, 0.032 and > 10 microM, respectively. Mean Ki values for the beta 2-antagonist ICI 118551 were 1.744, 1.243, and 0.019 microM. This result indicates that low concentrations of isoproterenol and norepinephrine stimulate lipolysis mainly via beta 1-adrenoceptors in dog fat cells. Inversely, the lipolytic effect of higher concentrations of agonists i.e., 1 microM isoproterenol and catecholamines, was weakly antagonized by CGP 20712A or ICI 118551 while the nonselective beta-antagonists bupranolol and propranolol suppressed the effects with the order of potency expected for a beta 3-adrenoceptor: bupranolol > propranolol. These data indicate 1) the presence of a functional beta 3-adrenoceptor that coexists with beta 1- and beta 2-adrenoceptors in dog fat cells; 2) a separation of the differential potencies of physiological amines in the activation of lipolysis through beta 1-, beta 2-, and beta 3-adrenoceptors; the lipolytic response initiated at low concentrations (submicromolar range) of norepinephrine is primarily mediated by the beta 1-adrenoceptor subtype; and 3) an activation of the beta 3-adrenoceptor that occurs at higher concentrations of catecholamines.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8096365&dopt=Abstract
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