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At least 343 records · Page 19Linked to original sources
PubMed1985

Involvement of epinephrine in the presynaptic beta adrenoceptor mechanism of norepinephrine release from rat hypothalamic slices.

Using high-performance liquid chromatography with electro-chemical detector, we measured field impulse (5 or 2 Hz)- and high K+ (20 mM)-evoked release of endogenous norepinephrine from rat hypothalamic slices. Release by impulses at 5 Hz was tetrodotoxin-sensitive and both types of release were Ca++-dependent. Isoproterenol (10(-10) to 10(-8) M) dose-dependently facilitated impulse-evoked release and l-propranolol (10(-8) M) shifted dose-effect curve of isoproterenol to the right. Atenolol (10(-8) to 10(-6) M) or butoxamine (10(-9) to 10(-8) M), beta-1 and beta-2-antagonist, respectively, dose-dependently antagonized the facilitatory effect of isoproterenol (10(-8) M). Tazolol (10(-8) to 10(-7) M), beta-1-agonist, and salbutamol (10(-10) to 10(-8) M), beta-2-agonist, dose-dependently increased impulse-evoked release. Epinephrine (10(-9) M) also facilitated impulse-evoked release and the action was antagonized by l-propranolol (10(-8) M). Isoproterenol (10(-8) M) also facilitated high K+-evoked release in the presence of tetrodotoxin (3 X 10(-7) M) to exclude possible involvement of axonal conduction or neuronal loops. This facilitatory effect was antagonized by l-propranolol (10(-8) M). l-Propranolol (3 X 10(-7) M) alone decreased release by impulses at 2 Hz, but the d-isomer produced no effect. When rats were pretreated with 2,3-dichloro-alpha-methylbenzylamine, an inhibitor of phenylethanolamine N-methyltransferase, the enzyme catalyzing the formation of epinephrine from norepinephrine, 80 mg/kg i.p. before decapitation, the l-propranolol-induced decrease was abolished completely.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

Antiarrhythmic effects of four different beta-adrenergic blockers in the mouse chloroform arrhythmia model.

The antiarrhythmic activity of four different beta-adrenergic blockers was assessed in the mouse chloroform arrhythmia model. ED50 values and 95% confidence intervals established by i.p. administration of drug were: propranolol (22.8, 10.9--67.0 mg/kg), sotalol (38.0, 15.9--58.5 mg/kg) and practolol (167, 111--235 mg/kg). Butoxamine provided some protection against the arrhythmia within a narrow dose range (53 to 79 mg/kg).

Adrenergic beta-Antagonists↗
PubMed1982

Theoretical and practical problems with the assessment of intrinsic efficacy of agonists: efficacy of reputed beta-1 selective adrenoceptor agonists for beta-2 adrenoceptors.

Agonist effects of the reputedly beta-1 selective adrenoceptor agonists prenalterol, dobutamine and tazolol were compared, in rat uterus, with those of the reportedly beta-2 selective agonist, terbutaline. Butoxamine was a simple competitive antagonist of responses to all agonists with a 10 to 16 times greater potency in rat uterus than in guinea-pig left atria. Similarly, atenolol was 50 to 80 times less potent as an antagonist of all agonists in rat uterus than guinea-pig left atria. The Schild regressions for both antagonists, when subjected to analyses of covariance of regression lines, yielded no evidence to suggest that the reputedly beta-1 selective agonists activated receptors different from those activated by terbutaline in rat uterus. These data indicated that the responses produced by these agonists in rat uterus were due to stimulation of beta-2 adrenoceptors under current classifications. An analysis of the relative intrinsic efficacy of prenalterol on beta-2 as opposed to beta-1 adrenoceptors indicated a nonselective efficacy at the receptor level. The implications of these data in terms of tissue-related efficacy (i.e., intrinsic activity) and receptor-related intrinsic efficacy (as defined by Furchgott) are discussed as a caveat to ascribing tissue selectivity to receptor selectivity without the appropriate data. Specifically, estimates of selective agonist efficacy at receptors should be made on the basis of selective intrinsic efficacy and not on measurements of agonists potency or maximal responses.

Adrenergic beta-Agonists↗
PubMed1983

[Pharmacological characterization of the adrenoceptors in the muscularis mucosae of the guinea-pig esophagus].

Pharmacological characteristics of the post-junctional adrenoceptors in the muscularis mucosae of the guinea-pig esophagus were examined in vitro. In the presence of propranolol (3 microM), all catecholamines, phenylephrine and methoxamine produced a weak contraction of the isolated muscularis mucosae. The order of potency of the contractile response was adrenaline greater than noradrenaline greater than methoxamine greater than phenylephrine and much weaker isoproterenol, dopamine and clonidine. The contractile responses to noradrenaline (10 microM) and adrenaline (10 microM) were markedly inhibited by phentolamine (3 microM), prazosin (3 microM), indomethacin (1 microM), aspirin (100 microM) and polyphloretin (30 microM), and slightly by yohimbine (3 microM). On the other hand, all catecholamines and terbutaline produced relaxation of the isolated muscularis mucosae which was maximally contracted with carbachol (3 microM) in the presence of phentolamine (10 microM), in a concentration-dependent manner. The order of potency of the inhibitory response was isoproterenol greater than noradrenaline greater than adrenaline and much weaker terbutaline and dopamine. The inhibitory responses to catecholamines were competitively antagonized by three beta blockers, being in the following order of potency as estimated by their pA2 values: propranolol greater than atenolol much greater than butoxamine. The pretreatment of the tissue with indomethacin (1 microM) did not modify the inhibitory responses to catecholamines. These results suggest that the guinea-pig esophageal muscularis mucosae has excitatory alpha 1 adrenoceptors and inhibitory beta 1 adrenoceptors, and the alpha 1, but not beta 1, adrenoceptors may link with the endogenous arachidonic acid cascade.

Adrenergic alpha-Antagonists↗
PubMed1984

[Effects of some drugs on plasma uric acid in rats--actions of catecholamines and beta-blocking agents].

Effects of catecholamines on plasma uric acid and allantoin levels were studied in oxonate-treated rats and non-treated rats. 1) In non-treated rats, epinephrine, isoproterenol and phenylephrine, which were injected intravenously, clearly increased plasma uric acid and allantoin, and norepinephrine had only a slight effect. The orders of potency to increase plasma uric acid and allantoin were epinephrine greater than isoproterenol greater than phenylephrine greater than norepinephrine. Beta-adrenoceptor agonists also increased plasma uric acid and allantoin in non-treated rats. The order of potency to increase plasma uric acid was isoproterenol salbutamol trimetoquinol greater than terbutaline, and that of potency to increase plasma allantoin was isoproterenol salbutamol greater than or equal to trimetoquinol greater than terbutaline. 2) In oxonate-treated rats, the four beta-adrenoceptor agonists (50 micrograms/kg, i.v.) markedly potentiated the hyperuricemic effect of oxonate. These effects of beta-adrenoceptor agonists were inhibited by propranolol (2.0 mg/kg. i.v.). In addition, the effect of isoproterenol was inhibited by butoxamine (1.0 mg/kg, i.v.), but not by atenolol (1.0 mg/kg, i.v.). These results suggest that hyperuricemia induced by catecholamines is closely related to beta 2-adrenoceptor action.

Adrenergic beta-Antagonists↗
PubMed1984

Effects of formoterol (BD 40A), a beta-adrenoceptor stimulant, on isolated guinea-pig lung parenchymal strips and antigen-induced SRS-A release in rats.

Formoterol was evaluated for its inhibitory effects on tissue tonus of the isolated guinea-pig lung parenchymal (peripheral airways) and tracheal (central airways) strips and on antigen-induced release of slow reactive substance of anaphylaxis (SRS-A) in the rat. Relaxant effects of formoterol in both parenchymal and tracheal strips were dose-dependent and were of similar potency. Formoterol was 44 and 100 times more potent than isoproterenol and salbutamol, respectively, in relaxing the parenchymal preparation. Propranolol, butoxamine and atenolol antagonized the relaxation of the parenchymal strips by formoterol in this order of decreasing potency; their slopes of regression line of the Schild plots were 0.809, 0.975 and 0.676, respectively. The inhibitory effect of intraperitoneally administered formoterol on (mouse) IgE-mediated SRS-A release in rat passive peritoneal anaphylaxis was 40 and 12200 times, respectively, more potent than those of salbutamol and disodium cromoglycate (DSCG). This action was antagonized by pretreatment with propranolol. In contrast to DSCG which dose-dependently inhibited histamine release, neither formoterol nor salbutamol was effective in inhibiting the release. The results indicate that formoterol potently relaxes the peripheral airways through stimulating the beta 2-adrenoceptors selectively as is the case in the central airways and that it significantly inhibits IgE-mediated SRS-A release through beta-adrenoceptor stimulation.

Adrenergic beta-Agonists↗
PubMed1980

Demonstration of beta-2 adrenergic receptors of high coupling efficiency in human neutrophil sonicates.

Using highly purified (greater than 95%) neutrophil (PMN) sonicates, we have studied the beta adrenergic (beta 1/beta 2) pattern of adenylate cyclase activation following agonist stimulation and have assessed the coupling characteristics of the beta adrenergic receptor to the adenylate cyclase enzyme. Adenylate cyclase was highly responsive to agonist activation, with peak isoproterenol (100 microM) stimulation resulting in the generation of 119 +/- 9.5 (mean +/- S.E.M.) pmol/mg/min cyclic AMP (224% above basal levels) compared to 171.7 +/- 8.6 following NaF (10 mM) stimulation. The agonist pattern of adenylate cyclase activation suggested the presence of beta-2 adrenergic receptors, since isoproterenol with a Kact of 0.7 microM was more potent than epinephrine (Kact = 8.5 microM) or norepinephrine (Kact = 90 microM). Butoxamine (beta-2 antagonist) was approximately 25 times more potent than practolol (beta-1 antagonist), with KDs of 0.75 microM and 17.5 microM, respectively. Receptor coupling efficiency was determined by measuring isoproterenol binding and adenylate cyclase activation with the same PMN sonicates and incubation conditions for each assay. The apparent KD for isoproterenol binding was 2.82 +/- 0.53 muM, the Kact was 0.47 +/- 0.05 muM, and the mean KD/Kact ratio was 6.5. Highly coupled receptor-enzyme systems have ratios greater than or equal to 1. Using sucrose gradient-purified PMN sonicates, we found that isoproterenol required the guanine nucleotides GTP or Gpp(NH)p to activate adenylate cyclase. The GTP effect on adenylate cyclase responsivenss to isoproterenol was associated with a 10-fold decrease in the isoproterenol binding affinity. These studies suggest that the human PMN has beta-2 adrenergic receptors which are highly coupled to the adenylate cyclase enzyme. We believe that this tissue offers a suitable model for the study of beta-2 adrenergic receptors and the mechanism of hormone-induced adenylate cyclase activation in man.

Adenylyl Cyclase Inhibitors↗
PubMed1982

Enhancement of prostaglandin output during activation of beta-1 adrenoceptors in the isolated rabbit heart.

The purpose of this study was to elucidate the type of adrenoceptor that mediates the effect of adrenergic stimuli on prostaglandin (PG) synthesis in the isolated rabbit heart and to determine the relationship of the released PGs to the mechanical changes elicited by catecholamines and stimulation of the cardiac sympathetic nerves. The output of 6-keto PGF1 alpha, PGE2 and PGF2 alpha was increased by electrical stimulation of the sympathetic nerves, norepinephrine, isoproterenol, dobutamine and angiotensin II, but not by phenylephrine or isoetharine. Propranolol or atenolol, but not phentolamine or butoxamine, blocked the output of PGs elicited by adrenergic stimuli. Indomethacin prevented the increase in PG formation caused by all stimuli. Moreover, the adrenergically induced release of PGs was not related to changes in heart rate, systolic tension or vascular tone elicited by the adrenergic stimuli. These data indicate that the adrenergically induced release of PGs in the isolated rabbit heart is due to the activation of beta-1 adrenoceptors and is independent of the mechanical effects produced by the adrenergic stimuli.

Angiotensin II↗
PubMed1981

The effects of adrenergic agonists and antagonists on vesicourethral smooth muscle of rabbits.

The effects of alpha and beta adrenergic agonists and antagonists on isolated smooth muscle preparations from the rabbit bladder body, bladder base and proximal urethra have been studied. The predominance of alpha receptors in the proximal urethra and the bladder base was observed via contraction of these areas by norepinephrine and blockade by phentolamine. Alpha receptor-mediated contractile activity could be unmasked in the bladder body when beta receptors were blocked with propranolol. Isoproterenol, 1 X 10(-10) to 3 X 10(-7) M, had a strong, dose-related relaxant effect on the bladder body, but little effect on the bladder base or proximal urethra. Selective beta-2 agonists such as terbutaline, salbutamol and ritodrine elicited tissue responses similar to those of isoproterenol. The pD2 values for isoproterenol, terbutaline, salbutamol and ritodrine were 8.59, 7.87, 7.34, and 6.52, respectively. Dobutamine, a selective beta-1 agonist, failed to cause significant relaxation of these tissues. The nonselective beta receptor blocker, propranolol, and the selective beta-2 receptor blocker, butoxamine, competitively antagonized the relaxant effects of the four active beta agonists; however, atenolol, a selective beta-1 receptor blocker, was inactive. On the basis of the selective action of these agonists and antagonists, we concluded that beta-2 receptors mediate relaxation of the vesicourethral smooth muscles of the rabbit and the participation of beta-1 receptors in the areas is insignificant.

Animals↗
PubMed1995

[The effect of noradrenaline and dopamine agonists and antagonists on oxygen consumption in some insect and crustacean species].

The effect of drugs on oxygen consumption in some invertebrate species (insect larvae and crustacea) was investigated. Insect larvae showed an increase in oxygen consumption under the influence of sympathomimetic drugs such as isoprenaline or orciprenaline which could be prevented by beta-receptor antagonists like propranolol or butoxamine. The drugs had no effect in crustacea. On the other hand, in these animals dopamine agonists of different chemical structure (amphetamine, apomorphine, lisuride) caused an increase in oxygen consumption whereas the dopamine antagonist metoclopramide had an opposite effect.

Animals↗
PubMedDate not supplied

Stereospecific binding of timolol, a beta-adrenergic blocking agent.

The beta-adrenergic blocking agent, timolol, appears to be bound to stereospecific as well as nonspecific sites in the particulate fraction (8500g pellet) of the heart, lungs, and brain, whereas the d-isomer of timolol was bound to nonspecific sites only. Timolol disappeared from the particulate fraction at a slower rate than did its optical isomer. At 1 hr after a 0.1-mg/kg dose, the concentration of the l-form in the lung was 1.8 times that of the d-isomer and at 3 and 4 hr the difference was at least 33-fold. The concentration of 14C-timolol in the particulate fraction of rat tissues was inhibited by iv administered timolol and by the l-isomer of propanolol, but not by their corresponding d-forms. Competition for binding sites was dose dependent. Pretreatment with timolol at 0.1 and 5.0 mg/kg reduced the binding of 14C-timolol (dose, 0.1 mg/kg) to lung tissue by 41% and 86%, respectively. In the heart and lung tissue of rats, racemic timolol, propranolol, bunolol, and bunitrolol were approximately equally effective in competing for the binding sites of 14C-timolol. Practolol and sotalol and the beta 2-selective agent butoxamine did not significantly inhibit the binding of 14C-timolol. Similar competition was also observed in the whole brain of rats. This report suggests that the stereospecific binding of timolol may be related to the beta-adrenoreceptor process.

Adrenergic beta-Antagonists↗
PubMed1997

Cardiotoxic effects of salmeterol in comparison with salbutamol on the isolated perfused Langendorff-heart of the rat.

beta 2-Adrenoceptor agonists used in the relief of bronchospasm have long been known to produce circulatory side-effects. Salmeterol (CAS 89365-50-4) is a novel long acting highly selective beta 2-agonist. We used the Langendorff-heart rat model (constant perfusion pressure) to compare the direct effects of salbutamol (CAS 18559-94-9, SAL) and salmeterol (SMT) on the cardiac performances and their toxic cardiac effects (induced by 3 mmol/l perfusate calcium). At the first step the concentration-effect curve was established for the maximal concentration (Cmax) of salbutamol leading to the maximal chronotropic effect on the heart for 20 min after a 20 min stabilization period (basal values). All hearts were consequently submitted to a 20 min Krebs-Henseleit perfusion in order to study the reversibility of the myocardial performances. The types of the myocardial and coronary beta-adrenoceptors involved in SAL (Cmax) effects were identified using a selective beta 1 (atenolol) and a beta 2 (butoxamine) antagonist. SAL induced an increase in the heart rate via a selective stimulation of the beta 1-adrenoceptors (beta 1-AR). SMT appeared to be more potent than SAL on the heart rate. Direct toxic drug effects on the heart appeared gradually with SAL whereas they appeared sharply at the highest concentration of SMT. The enzyme leakage observed during the recovery period was more pronounced with SMT than SAL. Perhaps, this phenomenon might be due to the lipophilicity of SMT. However, these direct cardiac effects of SMT have to be considered in association with its airway smooth muscle relaxant effect (therapeutic effect) which has been proven much more potent than those of SAL. Therefore SMT was less cardiotoxic than SAL at similar therapeutic concentrations.

Adrenergic beta-Agonists↗
PubMed1997

[Neurotransmitter-mediated regulatory mechanisms of axoplasmic transport--acetylcholine and adrenaline].

It has not been known whether or not the axoplasmic transport depends on regulatory influences mediated by neurotransmitters. The video-enhanced microscope technique has made it possible to visualize the real-time movement of micro-particles along axons and thus to observe its quick response to external signals. Using this technique, the effects of acetylcholine (ACh) and adrenaline on the axoplasmic transport in cultured cervical ganglion (SCG) cells were examined. Application of ACh inhibited the transport in both anterograde and retrograde directions. This effect was mimicked by the muscarinic receptor agonist arecoline, but not by the nicotinic receptor agonist nicotine. The response to ACh was inhibited by QNX (3-quinuclidinyl-xanthine-9-carboxylate), a muscarinic receptor antagonist. Immunocytochemistry and in situ hybridization with anti-muscarinic receptor subtypes compounds demonstrated the expression of m2 receptors on the SCG cell. Islet-activation protein (IAP), a G-protein inhibitor, completely blocked the suppressive effect of ACh. The protein kinase A (PKA) inhibitor KT-5720 induced a similar effect to that of ACh. In contrast to the effect of ACh, adrenaline increased both anterograde and retrograde transport. The beta 2-receptor agonist (albuterol), but not alpha-receptor agonists (phenylphrine and clonidine) or beta 1-receptor agonist (dobutamine), mimicked the effect of adrenaline. The beta 2-receptor antagonist butoxamine abolished the facilitatory response to adrenaline. Dibutyryl cyclic AMP, a membrane permeable cAMP, and forskolin, an activator of adenylyl cyclase, induced a similiar effect to that of adrenaline. These results suggest that 1) ACh, acting through m2-receptors, activates Gi-protein and thus inhibits cAMP synthesis, 2) adrenaline, acting through beta 2-receptors, increases intracellular cAMP concentration, and 3) these changes in cyclic AMP levels inhibit or enhance the activity of PKA to phosphorylate proteins related to the axoplasmic transport.

Acetylcholine↗
PubMedDate not supplied

Connective tissue activation. IX. Modification by pharmacologic agents.

Alpha- and beta-adrenergic blocking agents and imipramine inhibit the increased hyaluronate synthesis that may be induced in human synovial cultures by connective tissue activating peptide (CTAP). Considerations of drug concentration requirements, actions of analogues, and time studies all indicate that the adrenergic blockers do not act in this circumstance as conventional blockers of alpha or beta receptor sites. It is suggested that the membrane-stabilizing properties of these agents may be the important determinant for their limited "antiactivation" effect. Ethacrynic acid, a potent and more complete inhibitor of connective tissue activation, appears to act via a different mechanism.

Alprenolol↗
PubMedDate not supplied

Differential effects of propranolol on lymphocyte rosette formation and response to plant mitogens.

The effects of propranolol on various lymphocyte functions were studied to gain a better understanding of the recently demonstrated suppressive effect of propranolol on rheumatoid factor production. D- and L-propranolol at a concentration of 1 X 10(-4)M inhibited the formation of human EA rosettes. The inhibition occurred within one minute of adding the compounds, was reversible, and did not affect cell viability. Addtion of propranolol to preformed EA rosettes failed to disaggregate them. Patching and capping of SIg by an Fab'2 anti-IgG were inhibited at 2.5 X 10(-5)M and above. Propranolol at 2.5 X 10(-5)M also inhibited lymphocyte response to phytohemagglutinin and pokeweed mitogen without evidence of cell toxicity by trypan blue staining or absolute numbers of surviving cells. Congeners of propranolol with mainly beta adrenergic blocking properties did not show inhibitory effects. The inhibitory activities of propranolol are interpreted in terms of propranolol's membrane stablizing effects and ability to interfere with membrane receptor movement.

Animals↗