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At least 1,171 records · Page 65Linked to original sources
PubMed1980

Characterization of the receptor mediating the antianaphylactic effects of beta-adrenoceptor agonists in human lung tissue in vitro.

1 The rank order of potency of six beta-adrenoceptor agonists as inhibitors of the anaphylactic release of histamine from fragments of passively sensitized human lung in vitro was (--)-isoprenaline greater than (--) -adrenaline greater than (+/-)-salbutamol greater than (--)-noradrenaline greater than R0363 greater than H133/22. 2 The beta-adrenoceptor antagonists, propranolol, atenolol and H35/25, blocked the response to both (--)-isoprenaline and (+/-)-salbutamol competitively. Each antagonist gave similar pA2 values with both agonists. pA2 values were consistently at the high end of the range expected for interaction at a beta 2-adrenoceptor. 3 Practolol did not antagonize isoprenaline in a competitive manner but was a competitive antagonist of salbutamol with a pA2 at the high end of the range expected for interaction at a beta 2-adrenoceptor. 4 Data obtained with agonists are consistent with the receptor being of the beta 2-subtype. Data obtained with antagonists indicate a consistently higher affinity for the receptor than observed for the beta 2-subtype in other tissues but do not suggest a novel beta-adrenoceptor subtype on the mast cell of the human lung.

Adrenergic beta-Agonists↗
PubMed1981

Inhibition of lymphocyte capping and transformation by propranolol and related compounds.

1 The effects of propranolol on phytohaemagglutinin (PHA)-induced transformation of murine T lymphocytes and capping of anti-IgG on the surface of murine B lymphocytes have been examined. 2 A 50% inhibition of transformation was observed with 10(-5) M propranolol, whereas a higher concentration, of the order of 10(-3) M propranolol was required to inhibit capping by 50%. The (+)-and (-)-isomers of propranolol proved equipotent in these respects, and the relative potencies of selected analogues of propranolol (alprenolol, oxprenolol, metoprolol, practolol, and sotalol) coincided with their potencies as membrane stabilizers; however, lymphocyte transformation was consistently more sensitive than capping. 3 Similar effects were also seen with quinidine, chlorpromazine and lignocaine, and it was concluded that the inhibition of both lymphocyte functions was due to the membrane stabilizing actions of propranolol.

Adrenergic beta-Antagonists↗
PubMed1983

Additional evidence against universal modulation of beta-adrenoceptor responses by excessive thyroxine.

1 The effect of prolonged, excessive thyroxine on beta-adrenoceptor-mediated relaxation of guinea-pig trachea was studied. 2 Thyroxine did not significantly affect the potency of the beta 1-adrenoceptor agonist, noradrenaline, or the beta 2-adrenoceptor agonist, terbutaline. 3 Thyroxine did not significantly affect the apparent KB values of the selective beta 1-adrenoceptor antagonist, practolol, or the selective beta 2-adrenoceptor antagonist, butoxamine. 4 Thyroxine did not significantly affect the maximum response to noradrenaline. The maximum response to terbutaline in tissues from the thyroxine-treated animals was only slightly lower than the maximum response in tissues from paired control animals. 5 These results suggest that excessive thyroxine does not significantly affect the beta-adrenoceptor-mediated relaxation of guinea-pig trachea and that the reported modulation of beta-adrenoceptor-mediated responses in other tissues is specific for the given tissue rather than common to all beta-adrenoceptor systems.

Animals↗
PubMed1983

Beta 2-adrenoceptor blockade is the basis of guinea-pig bronchial hyper-responsiveness to leukotriene C4 and other agonists.

Four beta-adrenoceptor antagonists, namely (-)-propranolol, (+)-propranolol, ICI-118551 and (+/-)-practolol, were investigated for their effects on leukotriene C4 (LTC4)-induced bronchoconstriction in the anesthetized guinea-pig. (-)-Propranolol was also investigated for its effects on acetylcholine and histamine bronchospasm in the anaesthetized guinea-pig, and on LTC4-induced contractions of guinea-pig isolated trachea and lung parenchyma. The various beta-adrenoceptor antagonists potentiated, dose-dependently, the bronchoconstriction induced by threshold doses of LTC4 and the intensity of the potentiation correlated with the beta 2-blocking capacity possessed by the drugs. (-)-Propranolol potentiated the bronchospasm induced by threshold doses of acetylcholine and histamine but to a lesser degree than the LTC4-induced bronchospasm. The airway hyper-responsiveness induced by (-)-propranolol was unaffected by pretreatment with mepyramine, cyproheptadine, phenoxybenzamine, atropine or indomethacin. The airway hyper-responsiveness induced by (-)-propranolol persisted even in adrenalectomized or reserpine-treated guinea-pigs, although adrenalectomy induced some increase in airway responsiveness. (-)-Propranolol had no effect on LTC4, histamine and acetylcholine-induced contractions of isolated trachea and lung parenchyma. The results show that the airway hyper-responsiveness induced by beta-adrenoceptor antagonists generally correlates with their beta 2-blocking activity. The possibility remains that some other unknown mechanism(s) may also be implicated.

Adrenalectomy↗
PubMed1983

Cyclic adenosine 3',5'-monophosphate and beta-effects in rat isolated superior cervical ganglia.

Isoprenaline (0.01-1 microM) increased the amount of cyclic adenosine 3',5'-monophosphate (cyclic AMP) in rat isolated superior cervical ganglia by up to 10 times after 10 min application. Cyclic AMP levels returned to control values after 20 min washing. Salbutamol, in concentrations (1-100 microM) that depolarized the ganglion and facilitated submaximal transmission, did not significantly raise ganglionic cyclic AMP levels. The action of isoprenaline was antagonized by butoxamine (apparent KI approximately equal to 0.14 microM) and weakly by practolol (apparent KI approximately equal to 9.1 microM). The effect of 0.1 microM isoprenaline was also inhibited 94% by 100 microM of the adenylate cyclase inhibitor, 9-(tetrahydro-2-furyl)adenine (SQ 22,536). Exogenous dibutyryl cyclic AMP did not replicate the effects of isoprenaline on ganglionic d.c. potentials or submaximal transmission. The phosphodiesterase inhibitors theophylline, isobutylmethylxanthine or 4-(3,4-dibutoxybenzyl)-2-imidazolidinone (Ro 20-1724) did not potentiate these electrical responses to isoprenaline. The adenylate cyclase inhibitor, SQ 22,536, did not inhibit the electrical responses to isoprenaline. It is concluded that available evidence does not support the view that the ganglion depolarization or facilitation of submaximal transmission in rat isolated ganglia produced by isoprenaline are likely to be mediated by cyclic AMP.

Action Potentials↗
PubMed1986

Positive inotropic action of saponins on isolated atrial and papillary muscles from the guinea-pig.

The effects of several saponins of animal and plant origin on the contractile activity of atrial and papillary muscles of the guinea-pig were tested. In a concentration of 1 X 10(-5)M, holothurin-A (HL-A), holothurin-B, echinoside-A, echinoside-B and sakuraso-saponin (Saku) exhibited positive inotropic and chronotropic actions whereas desacyl-jego-saponin and ginsenoside-Rd did not. Saponins having a positive inotropic action caused haemolysis of rabbit erythrocytes whereas those without inotropic action did not cause haemolysis. The positive inotropic action of saponins was not affected by practolol, chlorpheniramine, cimetidine and indomethacin. Verapamil (10(-6)M) inhibited the inotropic actions due to HL-A and isoprenaline (10(-8)M) to the same extent but had a small effect on those due to ouabain (10(-7)M). In high K+ (30 mM K+) medium where the action potential and the contraction were depressed, HL-A, Saku and isoprenaline restored the action potential and the contraction of the 'slow response' type whereas ouabain failed to do so. In normal medium HL-A and Saku reduced the resting membrane potential by 15-20 mV. These results suggest that modification of the Ca channel is involved in the positive inotropic action of saponins.

Animals↗
PubMed1986

The effect of oxytocin on contractile responses and 45Ca movements in rat isolated aortic strips.

The effects of oxytocin (Oxt) on contractile responses and transmembrane Ca fluxes were studied in rat isolated aortic strips. Oxt (50-1000 mu ml-1) induced a dose-dependent contractile response and spontaneous myogenic activity. The Oxt-induced contractile response was not inhibited by pretreatment of aortic strips with phentolamine plus practolol, atropine, diphenhydramine plus cimetidine or indomethacin, but was significantly reduced by verapamil or deamino-ethyl-Oxt. The dose-response curve for Oxt was shifted upwards and to the left by increasing the Ca concentration of the medium from 1.8 to 4 mM. Oxt also shifted upwards the dose-response curve to Ca (1 to 5 mM) in aortic strips incubated in K depolarizing Ca-free media. Oxt increased the La3+-resistant 45Ca content without altering 45Ca efflux. The present results suggest that in rat isolated aortic strips Oxt produces a contractile response which, as previously found with other neurotransmitters, can be partly attributed to an increase of Ca influx through receptor-operated channels and to the release of Ca from intracellular stores.

Animals↗
PubMed1988

Catecholamines released from the adrenal medulla exert a compensatory, protective effect at beta 2-adrenoceptors against Paf-induced death in mice.

1. The effects of a number of drugs and experimental conditions, which inhibit or stimulate adrenergic function, were evaluated on platelet-activating factor (Paf)-induced death in conscious mice. 2. Adrenalectomy markedly potentiated Paf toxicity, while guanethidine and reserpine did not. However, reserpine, which produced a virtually complete depletion of catecholamines (CA) in cardiac tissue, was not able to reduce adrenal CA by more than 58%. Drugs which release noradrenaline from the adrenergic nerve terminals, such as tyramine and amphetamine, did not protect mice from Paf toxicity, while drugs or conditions which favour the release of CA from the adrenal medulla, such as urethane and cold-induced stress, did. 3. beta 2- and beta 1 + beta 2-adrenoceptor antagonists (ICI 118551, propranolol and nadolol), but not beta 1-antagonists (atenolol, practolol, metoprolol and CGP 20712 A), potentiated Paf toxicity at low doses; beta 2- and beta 1 + beta 2-agonists (salbutamol, fenoterol and isoprenaline), but not beta 1-agonists (prenalterol and tazolol) were potent inhibitors of Paf toxicity. alpha 1- and alpha 2-adrenoceptor agonists and antagonists did not exert significant effects. Propranolol did not appear to enhance the hypotensive action of Paf in pentobarbitone-anaesthetized mice. 4. It is concluded that manipulation of the release of CA from the adrenal medulla, but not from adrenergic nerves, has profound effects on Paf toxicity in mice. A number of considerations support the hypothesis that bronchoconstriction is a major determinant of Paf-induced death in mice.

Adrenal Cortex Hormones↗
PubMed1988

The mechanism of the inotropic action of striatoxin, a novel polypeptide toxin from a marine snail, in isolated cardiac muscle.

1. Striatoxin (StTX), a novel polypeptide from a marine snail, caused a dose-dependent increase in contractility in the isolated atria of guinea-pig and rat in the concentration-range of 2 x 10(-9) to 3 x 10(-8)M and 3 x 10(-6)M, respectively. 2. In guinea-pig atria, the StTX-induced inotropic effect was inhibited by tetrodotoxin but not by cimetidine or chlorpheniramine. Practolol, propranolol or reserpine caused only partial block of this inotropic action. 3. In isolated single cells from rat hearts, StTX caused an increase in the degree and the rate of contraction. 4. In guinea-pig atria, StTX provoked action potentials with a plateau phase of long duration without affecting the maximum rate of rise, the amplitude of action potential and the resting membrane potential. This prolongation was also reversed by tetrodotoxin. 5. In guinea-pig cardiac myocytes, whole-cell patch-clamp experiments showed that StTX slowed Na channel inactivation without affecting the time course of channel activation. The voltage dependence of Na currents was not altered by StTX. 6. The residual currents, but not peak currents were markedly enhanced by StTX. 7. These results suggest that StTX causes prolongation of the action potential duration probably due to slowed inactivation of Na inward currents and enhanced residual currents and that this may result in an increase in Ca2+ availability in cardiac muscle cells. This could explain the cardiotonic action of StTX.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1992

Beta-adrenoceptor agonist stimulation of acid secretion by rat stomach in vitro is mediated by 'atypical' beta-adrenoceptors.

1. A previous study showed beta-adrenoceptor agonists stimulated acid secretion by rat stomach in vitro. The receptors could not be classed as either the beta 1- or beta 2-subtype. This study examines the effect of 2 'atypical' beta-agonists on acid secretion. 2. Basal and isoprenaline-stimulated acid secretion were compared in tissues bathed either in HEPES/O2- or HCO3-/CO2-buffer. Basal secretion was underestimated in HCO3- by an amount equal to the rate of base section. Tissues responded well in HEPES buffer and there was no base secretion following acid inhibition with SCH 28080. HEPES was used for the study. 3. SR 58611A stimulated acid in a concentration-related way (0.1-5 microM). Maximum response at 1 microM was equal to the response to a maximal concentration of isoprenaline. BRL 37344 (1 microM) also stimulated to the same extent. 4. Responses to isoprenaline (5 microM) and SR 58611A (1 microM) were reduced by propranolol (10 microM) but not by alprenolol (10 microM) or by practolol (12.5 microM) plus ICI 118551 (1 microM). 5. Exposure to SR 58611A (1 microM) led to desensitization to isoprenaline but not to bethanechol (1 microM) or histamine (50 microM). 6. We conclude that a HEPES/O2-buffer is advantageous when measuring gastric acid secretion in vitro and the stimulatory effect of beta-adrenoceptor agonists is mediated by 'atypical' receptors.

Adrenergic beta-Agonists↗
PubMed1985

Functional beta 1- and beta 2-adrenoceptors in the human myocardium.

Functional beta-adrenoceptor populations in the human heart were studied in vitro in electrically-paced strips of the right auricular and ventricular myocardium. The relative potency of selected agonists in producing inotropic responses (Tmax, T'max) in the presence of blockers for neuronal and extraneuronal uptakes was found to be as follows: isoprenaline greater than noradrenaline = adrenaline = salbutamol greater than dobutamine. Prenalterol had a negative inotropic effect in these preparations. The selective beta 1-(practolol) and beta 2-(H 35/25) blockers reduced inotropic responses to adrenaline (Tmax, T'max) and noradrenaline (T'max) in the auricular strips. These results indicate the participation of beta 2-adrenoceptors in inotropic responses in the human auricular and ventricular myocardium. For comparison, inotropic responses of electrically-paced rat myocardium to beta-adrenergic agonists in the presence of blockers for neuronal and extraneuronal uptakes were likewise studied. The relative potencies for Tmax were: noradrenaline = adrenaline greater than prenalterol greater than dobutamine = salbutamol. Given the high relative potency of salbutamol in the human myocardial strips (analogous to that previous shown in the beta 2-dominated atria of the frog and trout) and the low relative potency of salbutamol in the rat tissue, these findings indicate a greater population of functionally active beta 2-adrenoceptors in the human than in the rat myocardium.

Adrenergic beta-Agonists↗
PubMed1975

Comparison of the beta-adrenoceptors in the myocardium and coronary vasculature of the kitten heart.

The relative potencies of (minus) noradrenaline, (minus)-adrenaline, (plus or minus)-isoprenaline and (plus or minus)-salbutamol have been assessed for their positive inotropic and chronotropic actions on kitten isolated atria. These relative potencies have been compared with those obtained for the relative coronary dilator potencies in two preparations. These were intact hearts perfused by Langendorff's method and isolated perfused coronary arteries from the kitten. The relative molar potencies for inotropic effects were noradrenaline 1: adrenaline1: iso-prenaline 7: salbutamol 0.6. The observed ratios for chronotropic effects were not significantly different from those for inotropic effects. The relative potencies of noradrenaline, adrenaline and isoprenaline as myocardial stimulants were similar to their relative potencies as coronary dilators in the intact heart. Similar relative potencies for noradrenaline and isoprenaline were also found in the isolated coronary artery but adrenaline was only one third as active as noradrenaline on this preparation. In both the intact heart and in the isolated coronary artery salbutamol was about one tenth as active as noradrenaline. It was therefore less active relative to noradrenaline as a coronary dilator than as a myocardial stimulant. In spite of these differences in relative potency ratios for myocardial and coronary dilator effects, similar dissociation constants (Kb values) for practolol against isoprenaline were found in driven atria and in isolated coronary arteries. Myocardial and coronary vascular beta-adrenoceptors thus can both be placed in the general classification of beta1-adrenoceptors.

Adrenergic beta-Antagonists↗
PubMed1977

Analysis of the beta-receptor mediated effect on slow-contracting skeletal muscle in vitro.

Subtetanic contractions of the guinea-pig isolated soleus, a slow-contracting skeletal muscle, were evoked by transmural field-stimulation. Isoprenaline caused a dose-dependent depression of the contractions. This effect was inhibited by propranolol and H 35/25 (1-(p-tolyl-2-isopropylamino-1-propanol) but not by practolol. Similar results were obtained for terbutaline. Tazolol and H 80/62 (1-isopropylamino-3-(p-hydroxyphenoxy)-2-propanol (HCl), selective beta1-agonists, had no effect per se but inhibited the effect of terbutaline. Adrenaline, noradrenaline, and dopamine all caused a dose-dependent decrease in the force of the soleus contractions, their potencies being in that order. Tyramine did not appreciably affect the contractions nor did it inhibit the effect of terbutaline. Pretreatment with reserpine, if anything, increased the response to terbutaline. It is concluded, in conformity with previous in vivo studies, that the adrenergic receptor mediating the effect on the soleus muscle contractions is of the beta2-type. Indirect sympathomimetic effects do not contribute to the responses observed on the isolated soleus muscle.

Adrenergic beta-Antagonists↗
PubMed1977

Evidence from agonist and antagonist studies to suggest that the beta1-adrenoceptors subserving the positive inotropic and chronotropic responses of the heart do not belong to two separate subgroups.

The positive inotropic and chronotropic responses of guinea-pig isolated left and right atria to 17 sympathomimetic amines were examined under conditions selected to control the pharmacological environment. Each agonist was compared with (--)-isoprenaline as the reference by constructing dose-response curves. Equiactive molar concentration ratios relative to (--)-isoprenaline were calculated at the EC50 for rate and tension responses. Statistical analysis revealed that (--)-noradrenaline and (+/-)-alpha-methylnoradrenaline were tension selective whereas (+/-)-alpha-ethylisoprenaline and N-methyldopamine were rate selective relative to (--)-isoprenaline. However, no structural trends emerged. The rank order of potency varied slightly between rate and tension, but an analysis of the regression and correlation coefficients indicated respectively that the equiactive molar concentration ratios and the rank orders could be considered identical on rate and tension. Antagonism of the (--)-isoprenaline-induced rate and tension responses by acebutolol, atenolol, practolol and propranolol was assessed from the pA2 values which were almost identical for both parameters with each antagnosti. It is concluded that the beta1-adrenoceptors mediating the positive inotropic and chronotropic responses do not warrant subdivision into two separate groups.

Adrenergic beta-Agonists↗
PubMed1984

Effect of dopamine on dog distal colon in-vitro.

The effects of dopamine, isoprenaline, adrenaline and noradrenaline in dog isolated colon strips were studied. All these drugs produced in the preparation relaxations which were inhibited by propranolol and sotalol or, in the case of noradrenaline, by a mixture of propranolol and phentolamine. A selective beta 1-adrenergic antagonist, practolol, had the same inhibitory effects on the relaxations induced by all the agonists, suggesting the existence of beta 1- and beta 2-adrenoceptor subtypes in the dog distal colon. There is no evidence for the presence of specific dopaminergic receptors in this preparation.

Animals↗
PubMed1984

Characterization of beta-adrenoceptors mediating relaxation of the guinea-pig ileum.

Relaxation responses to sympathomimetic amines were recorded in potassium-contracted segments of guinea-pig ileum. Experiments were performed in the presence of phentolamine (5 X 10(-6) M) to eliminate beta-adrenoceptor-mediated effects. Metanephrine (10(-5) M) and desmethylimipramine (5 X 10(-7) M) were also present to prevent extraneuronal and neuronal uptake respectively. A potency order (-)-isoprenaline greater than (-)-noradrenaline greater than (-)-adrenaline was established, indicating a beta 1-adrenoceptor involvement for this relaxation. The potency of salbutamol (beta 2-selective) relative to isoprenaline in the ileum compared closely with its relative potency in isolated cardiac tissues (beta 1) but differed significantly from the value in lung parenchymal strips and vas deferens (beta 2). The pA2 values for antagonism of selective agonists (-)-noradrenaline (beta 1-selective) and fenoterol (beta 2-selective) by practolol (beta 1-selective) were identical, indicating a single beta 1-adrenoceptor population. The pA2 values for antagonism of these agonists by ICI 118,551 (beta 2-selective) were also identical and compatible with a beta 1-adrenoceptor population. Relaxation of the guinea-pig ileum is therefore mediated via a homogeneous population of beta 1-adrenoceptors.

Albuterol↗
PubMed1985

The absorption of beta-adrenoceptor antagonists in rat in-situ small intestine; the effect of lipophilicity.

Intestinal absorption characteristics of eleven beta-adrenoceptor antagonists were measured by monitoring their disappearance from in-situ intestinal loops in the anaesthetized rat. All have basic pKa values of around 9.5 (with the exception of sotalol) but show a wide range of lipophilic character (octanol-water log P values from -0.79 to 3.65). The results show two types of absorption behaviour, indicating different mechanisms for 'hydrophilic' and 'lipophilic' beta-adrenoceptor antagonists. The four most hydrophilic molecules (sotalol, atenolol, nadolol and practolol) show virtually identical absorption rate constants. Absorption is slow and relative rates in jejunum (mean pH 6.5) and ileum (mean pH 7.3) are not consistent with pH-partition (jejunum greater than or equal to ileum). The more lipophilic members of the series (pindolol, timolol, metoprolol, oxprenolol, alprenolol and propranolol) are all absorbed much more rapidly. Absorption rate constant rises rapidly with log P and the expected pH effects are seen (ileum greater than jejunum). Acebutolol shows anomalously slow absorption for its log P value.

Adrenergic beta-Antagonists↗
PubMed1986

Effect of adrenergic drugs on the isolated colon of Rhesus cynomolgus.

The effects of adrenaline, noradrenaline, isoprenaline and dopamine were studied on the longitudinal muscle of the ascending and descending colon of the rhesus monkey. All these drugs induced a relaxation of the preparation, dopamine being the less active agonist. The responses seem to be the result of beta 2-adrenoceptor stimulation since their inhibition by practolol (beta 1) is weaker than their inhibition by propranolol (beta 1 and beta 2 dopaminergic). There is no evidence for the presence of dopaminergic receptors in this preparation.

Animals↗