Drugs online research references
J Physiol. 1984 Nov;356:335-48.
Beta-adrenergic receptor mechanisms in rat parotid glands: activation by nerve stimulation and 3-isobutyl-1-methylxanthine.
Fuller CM, Gallacher DV.
The technique of electrical field stimulation (e.f.s.) was employed in conjunction with selective pharmacological antagonists to specifically investigate the role of endogenous neurotransmitter(s) in the activation of beta-adrenergic receptor mechanisms in isolated parotid gland segments of the rat. The field-stimulus-induced amylase release due to beta-adrenergic receptor activation was characterized as that persisting in the presence of atropine (10(-5) M) and phentolamine (10(-5) M) and susceptible to blockade by propranolol (5 X 10(-6) M), i.e. combined beta 1- and beta 2-receptor blockade. The selective beta 1-receptor antagonist metoprolol (10(-5) M) was as effective as propranolol in blocking the beta-mediated enzyme release. The selective beta 2-receptor antagonist, H35/25 (10(-5) M) did not significantly affect the field-stimulus-induced amylase release. In the absence of any phosphodiesterase inhibitor the levels of cyclic AMP in the tissues were close to the limit of detection. Field stimulation was however associated with a fourfold increase in cyclic AMP. By comparison isoprenaline (10(-5) M) gave rise to a tenfold increase in cyclic AMP. The changes in cyclic AMP metabolism, in response to both field stimulation and isoprenaline, were greatly enhanced in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). The field-stimulus-induced increase in cyclic AMP was abolished by the beta 1-adrenergic receptor antagonist, metoprolol, but persisted in the presence of the beta 2-adrenergic antagonist, H35/25. IBMX was found to have a potent direct effect on amylase release. IBMX (10(-3) M) also gave rise to a tenfold increase in cyclic AMP. IBMX is then as effective as 10(-5) M-isoprenaline in stimulating both enzyme secretion and cyclic AMP metabolism. The secretory response to IBMX was unaffected by beta-adrenergic blockade by propranolol, was independent of extracellular calcium and did not give rise to 86Rb+ efflux. Importantly, isoprenaline (10(-5) M) failed to evoke any significant increase in amylase release if introduced during sustained superfusion of IBMX, yet it is in such protocols that the greatest changes in cyclic AMP metabolism are seen. The study clearly demonstrates that the beta-adrenergic-receptor-regulated amylase release in response to nerve stimulation is mediated predominantly, if not exclusively, by the beta 1-receptor subtype.(ABSTRACT TRUNCATED AT 400 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6084058&dopt=Abstract
Prostaglandins. 1987 Jan;33(1):25-35.
Adrenergic receptors mediating prostaglandin production in the rabbit vas deferens.
Trachte GJ.
Contractile and prostaglandin E (PGE)-producing effects of adrenergic agonists were compared in the rabbit isolated vas deferens to determine which adrenergic receptor(s) potentially could mediate neural responses. Additionally, interactions among receptors were elucidated by comparing responses to norepinephrine, phenylephrine and isoproterenol to those in the presence of selective adrenergic agonists or antagonists. Norepinephrine increased the force of muscle contraction and the immunoassayable PGE concentrations in a concentration-dependent manner with EC50's of 55 +/- 8 and 112 +/- 39 microM, respectively. Propranolol (10 microM) enhanced the contractile effects of norepinephrine (p less than 0.01) whereas yohimbine (100 microM) or prazosin (1 microM) reduced norepinephrine-induced contractions and PGE production (p less than 0.01). Propranolol did not alter the PGE production induced by norepinephrine. Metoprolol (100 microM) also enhanced contractile effects of norepinephrine (p less than 0.05). The beta adrenergic agonist, isoproterenol (100 nM), decreased the contractile, but not the PGE-producing, effects of phenylephrine (p less than 0.001). Isoproterenol, given alone, increased PGE concentrations and inhibited electrically-induced force generation in a concentration-dependent manner. These results are consistent with the presence of alpha receptors on the vas deferens which mediate smooth muscle contraction and PGE generation. Beta receptors which mediate relaxation and PGE production also are present. Tentative identification of the beta receptor subtype revealed the presence of a beta 1 receptor.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2884695&dopt=Abstract
Anaesthesiol Reanim. 2000;25(4):102-4.
[Effect of migraine medications on monocyte chemotaxis] .
[Article in German]
Krumholz W, Szalay G, Ogal H, Menges T.
Abteilung Anasthesie und Operative Intensivmedizin, Bethlehem-Krankenhauses Stolberg/Rheinland.
Monocytes play an important role in humoral as well as in cell-mediated immunity. In the present study, the influences of the anti-migraine preparations metoprolol, propranolol, metoclopramide, acetylsalicylic acid, dihydro-ergotamine and sumatriptan on monocyte chemotaxis were examined in vitro. First, mononuclear cells were isolated by centrifugation from venous blood samples obtained from 10 healthy male volunteers. Chemotaxis was determined using a microchemotaxis chamber. While metoprolol, metoclopramide, dihydroergotamine and sumatriptan did not influence monocyte chemotaxis, high doses of propranolol and acetylsalicylic acid caused a significant (p < or = 0.001) inhibition of this important cellular function. Therefore, it is quite possible that both drugs produce adverse immunological effects in vivo in cases of high dosage or obstruction of elimination.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11132397&dopt=Abstract
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