Drugs online research references
Gen Pharmacol. 1987;18(1):25-31.
Partial agonists at guinea-pig atrial beta-adrenoceptors display relaxation responses in the guinea-pig ileum independent of beta-adrenoceptor stimulation.
Grassby PF, Broadley KJ.
The beta-adrenoceptor mediated responses of oxyfedrine, ritodrine, tazolol, prenalterol, salbutamol and carteolol were examined on guinea-pig left and right atrial and ileal preparations. All agonists tested in left and right atrial preparations were partial agonists relative to isoprenaline. All agonists with the exception of salbutamol, which appeared a full agonist, produced relaxation responses significantly greater than isoprenaline in ileal preparations. The response to ritodrine in the ileum was not influenced by practolol, in a concentration which antagonized the responses of ritodrine in the right atria. The response of the ileum to beta-adrenoceptor antagonists of varying lipophyllicity was examined. Propranolol and pindolol both produced relaxation responses relative to their lipophyllicities. No relaxation was observed to atenolol, which exhibits very low lipophyllicity. It is concluded that beta-adrenoceptor agonists exhibit a substantial relaxation of guinea-pig ileum that is independent of beta-adrenoceptor stimulation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2881833&dopt=Abstract
Jpn J Pharmacol. 1983 Feb;33(1):219-26.
Drug-induced inhibition of guinea pig platelet aggregation unrelated to their beta-adrenolytic actions.
Iwamura M, Ishimori T, Makino M, Yasuda K, Izumi A, Himori N.
Inhibitory actions on adenosine diphosphate (ADP)-induced platelet aggregation of atenolol, dl- and d-D-32, IPS-339, pindolol and propranolol were investigated in guinea pigs for the purpose of obtaining a clue about a possible mechanism for the disaggregatory phenomenon of beta-adrenoceptor blocking agents. The effects of verapamil and procaine on guinea pig platelet aggregation were also examined. All of these agents including verapamil and procaine showed a dose-dependent inhibitory effect on platelet aggregation, and their relative potencies determined on the basis of the molar concentrations producing a 50% inhibition of ADP-induced aggregation were in descending order: IPS-339 greater than propranolol greater than verapamil greater than dl-D-32 not equal to d-D-32 greater than pindolol greater than procaine greater than atenolol. This order of relative potencies of the inhibitory actions of these test compounds on platelet aggregation was well correlated to those of local anaesthetic action in guinea pigs (r = 0.932, P less than 0.01) and lipophilicity (r = -0.899, P less than 0.01), while it did not agree with the orders of potency of beta-adrenoceptor blocking action, intrinsic sympathomimetic action and vasodilator action. From these results, it may be reasonable to propose that inhibitory actions of beta-adrenoceptor blocking agents and local anaesthetics on platelet aggregation are caused through the same mechanism or through a very similar one.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6135813&dopt=Abstract
Br J Clin Pharmacol. 1984;17 Suppl 1:51S-57S.
The interaction between H2-receptor antagonists and beta-adrenoceptor blockers.
Mutschler E, Spahn H, Kirch W.
The degrees of interactions between the H2-receptor antagonists, cimetidine and ranitidine, and several beta-adrenoceptor blockers were investigated in healthy volunteers following 7 days of oral monotherapy with penbutolol, propranolol, metoprolol, pindolol and atenolol, and after co-administration with each of the H2-receptor antagonists. The kinetic parameters of unmetabolised penbutolol and penbutolol glucuronide were unaffected, whereas the levels of 4-hydroxypenbutolol and 4-hydroxypenbutolol glucuronide were significantly reduced. Furthermore, cimetidine led to a marked increase in propranolol and metoprolol plasma levels. During co-administration with cimetidine, pindolol plasma levels were only slightly raised, whereas the pharmacokinetics of atenolol were not affected. With regard to pharmacodynamics, the inhibition of exercise-induced tachycardia by each of the beta-adrenoceptor blockers was not affected by cimetidine. Ranitidine did not alter atenolol plasma levels, but did raise the peak plasma concentration of metoprolol by about 30%. It is concluded that cimetidine interactions do occur and can be predicted for substances metabolised by the cytochrome P-450 pathway.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6146340&dopt=Abstract
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