Drugs online research references
Pharmacol Biochem Behav. 1993 Apr;44(4):869-75.
Effects of escapable and inescapable foot-shock on rat atrial beta-adrenoceptors.
Bassani RA, Bassani JW.
Dep. Engenharia Biomedica, Faculdade de Engenharia Eletrica, Universidade Estadual de Campinas, Sao Paulo, Brazil.
The chronotropic responsiveness to norepinephrine (NE) and isoproterenol (ISO) was determined in right atria isolated from rats submitted to repeated escapable or inescapable foot-shock. Significant postjunctional supersensitivity to ISO, but not to NE, was observed in both groups. No significant change in the pA2 value of metoprolol (a selective beta 1-adrenoceptor antagonist) was detected. However, a decrease of the maximum response to soterenol, a partial agonist at beta 1-adrenoceptors, occurred only after inescapable foot-shock. The enhanced sensitivity to ISO was abolished by butoxamine (a selective beta 2-adrenoceptor antagonist) and accompanied by a marked increase in the pA2 value of this antagonist. We conclude that the ability to control the shock prevented the down-regulation of the pacemaker beta 1-adrenoceptors but not the increased participation of beta 2-adrenoceptors in the response of the rat sinoatrial node to catecholamines after repeated foot-shock.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8385784&dopt=Abstract
Clin Exp Hypertens A. 1985;7(2-3):159-66.
Adrenergic and vagal influences on blood pressure variability.
Clement DL, De Pue N, Jordaens LJ, Packet L.
The present paper reviews our recent studies set up to define the role of sympathetic and vagal nervous influences on blood pressure variability. Blood pressure and its variability was measured in men by Arteriosonde or by Portometer (the latter recording 12 hours ambulatory blood pressure) and in the dog by intraarterial recordings. It was shown that sympathetic nerves do not influence variability as no change was seen with drugs acting on either beta (atenolol, metoprolol, propranolol) or alpha adrenergic receptors (prazosin, phentolamine, guanfacine). Also no correlation was found with plasma catecholamines or sympathetic function tests. By contrast, clear inhibition was demonstrated with atropine indicating an important role of vagal nerves on variability. However, in men, inhibition was not complete with atropine; thus, also other mechanisms play a role but these are, at present, largely unknown.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2860986&dopt=Abstract
Biochem Pharmacol. 1993 Jun 22;45(12):2441-7.
Effects of adrenergic agonists and antagonists on the metabolism of [1-14C]oleic acid by rat hepatocytes.
Olubadewo JO, Heimberg M.
Department of Pharmacology, University of Tennessee, Memphis 38163.
The possibility that the antihypertensive adrenoceptor antagonists (propranolol, phentolamine and metoprolol) may alter hepatic lipid metabolism was examined in freshly dispersed rat hepatocytes with [1-14C]oleate. Propranolol (1.8 x 10(-4) M) and phentolamine (1.4 x 10(-4) M) increased incorporation of [1-14C]oleate into cholesteryl esters by 51 and 92%, respectively, and decreased ketogenesis by 46 and 62%, respectively. While neither drug affected incorporation into total phospholipid, propranolol decreased triglyceride synthesis by 37%. These effects of propranolol and phentolamine may not occur through beta- or alpha-receptor inhibition since neither epinephrine nor norepinephrine reversed the effects of the adrenoceptor antagonists. Although epinephrine and norepinephrine per se did not alter the incorporation of [1-14C]oleate into triglyceride, phospholipid, cholesteryl esters or ketone bodies, they stimulated the production of 14CO2 (control 5.6 +/- 1.3; epinephrine 7.6 +/- 1.1; norepinephrine 9.1 +/- 0.2 nmol oleate incorporated/mg protein), and these effects were reversed by phentolamine and propranolol. The data suggest that adrenoceptor antagonists exert direct effects on hepatic metabolism of oleate.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8328982&dopt=Abstract
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