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At least 19 recordsLinked to original sources
PubMed1977

Regulation of intracellular cyclic GMP and cyclic AMP levels in mouse lung fragments by disodium cromoglycate, beta-adrenergic agonists, cholinergic activators, and histamine.

The effects of adrenergic and cholinergic agents as well as the effects of disodium cromoglycate (DSCG) on the levels of cyclic AMP and cyclic GMP in mouse lung fragments were studied. Levels of cyclic AMP were enhanced by two of the known beta-adrenergic agonists, epinephrine and isoproterenol. This increase was abolished by propanolol, a recognized beta-adrenergic antagonist. Disodium cromoglycate, a proposed inhibitor of phosphodiesterases, alone caused a slight, significant increase in cyclic AMP. However, in the presence of epinephrine, levels of cyclic AMP were potentiated by DSCG. DSCG behaves, therefore, as a typical cyclic AMP phosphodiesterase inhibitor. Cyclic GMP levels were increased by carbachol, acetylcholine, and the phosphodiesterase inhibitor, aminophylline, but not by DSCG, or beta-adrenergic agonists.

Adrenergic beta-Agonists↗
PubMed1979

Isolated lung strips of guinea pigs: responses to beta-adrenergic agonists and antagonists.

Isolated lung strips of guinea pigs were examined as an in vitro model for assessing the direct effect of beta-adrenergic drugs at the level of peripheral airways. Changes in intrinsic tone of thin strips of lung parenchyma were measured with an isometric force transducer. Isoproterenol, a nonselective beta-adrenergic agonist, and several beta-adrenergic agonists, soterenol, salbutamol, metaproterenol and ritodrine elicited a dose-related relaxation of lung strip. Responses to isoproterenol were antagonized by propranolol and the selective beta blocking agents butoxamine (beta2) and practolol (beta1). These results were compared to data obtained with the same compounds on isolated guinea pig atria. All agonists except ritodrine were full agonists in the lung strip whereas isoproterenol and metaproterenol were the only full agonists in the atrial preparation. In the atria, practolol was a more effective blocker of isoproterenol responses than butoxamine, and the reverse was true for the lung strip.

Adrenergic beta-Agonists↗
PubMed1977

The effects of adrenergic agonists and blockers on antigen-induced DNA synthesis in vitro.

The effects of both alpha and beta adrenergic agonists and blockers on antigen-stimulated DNA synthesis in human lymphocyte cultures were studied. Results show that antigen-induced responses were enhanced by the presence of the beta blockers, propranolol and dichloroisoproterenol, and that this effect appeared to be specific blocking of the lymphocyte beta receptor since D (+) propranolol, a compound devoid of such acitvity, has no effect. Similarly, and alpha adrenergic agonist such as norepinephrine enhanced lymphocyte responsiveness.

Adrenergic Agonists↗
PubMed1978

Analysis of the effect of adrenergic agonists on longitudinal and circular smooth muscle of the terminal ileum of the guinea pig.

On the isolated longitudinal smooth muscle of the guinea pig's terminal ileum, in the presence of naphazoline, synephrine, pholedrine and ephedrine showing no adrenergic agonist activity, the dose-response curves of adrenaline and noradrenaline was found to be shifted to the right. Metanephrine, normetanephrine, and 3-methoxy-4-hydroxyphenylethylamine exhibited no alpha adrenergic agonist activity. On the circular smooth muscle of the terminal ileum the alpha adrenergic agonists studied elicited the same responses as on the longitudinal smooth muscle.

Animals↗
PubMed1979

Effects of adrenergic agonists on the oxygen uptake and amylase output in rat submandibular gland slices.

Oxygen uptake and amylase output in rat submandibular gland slices were measured by utilizing adrenergic agonists. Adrenaline, noradrenaline and isoproterenol significantly stimulated the oxygen uptake and amylase output. In the presence of propranolol or phenoxybenzamine, adrenaline-stimulated oxygen uptake was obviously blocked. Adrenaline-stimulated amylase output was inhibited by propranolol, but was not inhibited by phenoxybenzamine. The increase in oxygen uptake by nornol-stimulated oxygen uptake and amylase output were strongly inhibited by propranolol. The oxygen uptake due to isoproterenol was little affected by phenoxybenzamine. These results suggest that the increase in oxygen uptake seen with adrenergic agonists is mediated by both alpha- and beta-receptors, and that the amylase output is evoked through the stimulation of beta-receptors.

Adrenergic Agonists↗
PubMed1976

Effect of beta-adrenergic agonists aerosolized by freon propellant on tracheal mucous velocity and cardiac output.

The present study was designed to assess the effects of two beta-adrenergic agonists, isoproterenol sulfate and carbuterol hydrochloride, and aerosolized Freon propellant (a mixture of Freon II, Freon 12, and Freon 114) on tracheal mucous velocity and cardiac output in anesthetized dogs. Five groups of ten animals each received the following dosages of aerosols: Freon, 20 puffs; isoproterenol, four puffs; carbuterol, four puffs; isoproterenol, 20 puffs; and carbuterol, 20 puffs. The puff was delivered by a standard metered aerosol; each puff of isoproterenol spray contained 75 mug of isoproterenol sulfate, and each puff of carbuterol spray contained 100 mug of carbuterol hydrochloride. Tracheal mucous velocity was not changed by receiving Freon, but administration of both isoproterenol and carbuterol caused a significant increase in this measurement, with peak increases ranging from 74 to 111 percent above control values. The duration of action for four and 20 puffs of isoproterenol and for four puffs of carbuterol was two hours. Twenty puffs of carbuterol increased tracheal mucous velocity for three hours. Administration of carbuterol effected a slightly larger increase in cardiac output than isoproterenol. The duration of action for the increased cardiac output was shorter than the duration of action for the increased tracheal mucous velocity. These studies indicate that beta-adrenergic agonists may have an important role in improving mucous transport in patients with chronic obstructive pulmonary disease in whom mucociliary clearance is depressed.

Adrenergic beta-Agonists↗
PubMed1977

Modulation of in vitro erythropoiesis. The influence of beta-adrenergic agonists on erythroid colony formation.

Canine marrow erythroid colony growth is enhanced by agents linked to the adenyl cyclase/cyclic AMP (cAMP) system, including cAMP, a phosphodieterase inhibitor (RO-20-1724), cholera enterotoxin, and beta-adrenergic agonists. The adrenergic effect is mediated by receptors having beta2-subspecificity. These receptors are distinct from putative receptors for erythropoietin and those acted upon by cholera enterotoxin. In addition, the population of cells most responsive to beta-agonists is distinct from the majority of erythropoientin-responsive cells, perhaps representing a subpopulation of this class of cell. This demonstration of an adenyl cyclase-linked mechanism regulating mammalian erythroid colony growth provides a model for the modulation by other hormones or small molecules of in vitro and, perhaps, in vivo erythropoiesis.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed1977

Adrenergic agents. 8.1 Synthesis and beta-adrenergic agonist activity of some 3-tert-butylamino-2-(substituted phenyl)-1-propanols.

Replacement of the benzylic hydroxyl group of N-tert-butylnorepinephrine with a hydroxymethyl substituent affords a propanolamine homologue which retains a high degree of beta-adrenergic agonist activity. As modification of the meta substituent of catecholic ethanolamines, such as N-tert-butylnorepinephrine, often provides compounds that exert a more pronounced effect in relaxing tracheobronchial smooth muscle (beta2-adrenergic agonist) than in stimulating cardiac muscle (beta1-adrenergic response), a series of 3-tert-butylamino-2-(3-substituted 4-hydroxyphenyl)-1-propanols was prepared. The 3-meta substituents included HOCH2 (1b), H2NCONH (1c), MeSO2NH (1d), H (le), and NH2 (1f). These phenylpropanolamine derivatives were compared with their phenylethanolamine counterparts in in vitro tests that measure the ability of these compounds to relax spontaneously contracted guinea pig tracheal smooth muscle (a measure of potential bronchodilating activity) and to increase the rate of contraction of a spontaneously beating guinea pig right atrial preparation (an indicator of potential cardiac stimulating activity). In these tests all of the propanolamine derivatives included in the study were less potent than their ethanolamine relatives. In both series replacement of the catecholic m-hydroxyl group with the indicated substituents usually resulted in compounds with increased selectivity for tracheobronchial vs. cardiac muscle.

Adrenergic beta-Agonists↗
PubMed1977

Adrenergic agents. 4. Substituted phenoxypropanolamine derivatives as potential beta-adrenergic agonists.

A series of 1-(substituted phenoxy)-3-(tert-butylamino)-2-propanols in which the ring substituents were 3,4-dihydroxy (6f), 3- and 4-hydroxy (6g and 6h, respectively), 3-hydroxy-4-methylsulfonamido (6i), its 3,4-transposed isomer (6j), and 4-methylsulfonylmethyl (6k) was prepared and examined for beta-adrenergic agonist and/or antagonist properties. Two of these compounds, 6f and 6j, were potent beta-adrenoreceptor agonists in in vitro tests that measure a compound's ability to relax guinea pig tracheal smooth muscle and to increase the rate of contraction of guinea pig right atria. Several compounds had a dose-dependent effect. Although they produced potent beta-adrenergic agonist activity at low concentrations, 6g, 6h, and 6j antagonized the effects of a standard beta-adrenoreceptor agonist at higher concentrations. The methylsulfonylmethyl derivative 6k produced beta-adrenergic blocking effects as demonstrated by attenuation of isoproterenol-induced increases in the rate of contraction of an isolated rabbit heart preparation. On the basis of these pharmacological results, coupled with NMR spectral data, it appears that the previous suggestion that aryloxypropanolamines interact with beta-adrenocreceptors as a consequence of their ability to assume an orientation in which the benzene ring the ethanolamine moieties can be superimposed on those of corresponding adrenergic phenylethanolamines is invalid. An alternative "bicyclic" rigid conformation involving two intramolecular hydrogen bonds in the protonated form of the aryloxypropanolamines is suggested to account for the similar beta-adrenoreceptor activity of these compounds and related phenylethanolamines.

Adrenergic beta-Agonists↗
PubMed1978

Membrane potential and resistance changes induced in salivary gland acinar cells by microiontophoretic application of acetylcholine and adrenergic agonists.

The effects of microiontophoretic applications of catecholamines and acetylcholine on parotid acinar cell membrane potential and resistance were investigated using intracellular microelectrode recording in superfused segments of mouse parotid or rat submandibular glands. Short pulses of acetylcholine and alpha-adrenergic agonists had similar effects, consisting of a marked decrease in membrane resistance accompanied by an initial depolization or hyperpolarization depending on the level of the resting membrane potential. This initial response was followed by a slow hyperpolarization occurring at a time when the resistance was increasing towards the prestimulation level. The equilibrium potential for the initial potential change caused by excitation of the cholinergic receptors was investigated directly by setting the membrane potential at different levels by injecting direct current and stimulating the same cell repeatedly with equal doses of acetylcholine. The equilibrium potential was found to be about -55 mV. The delayed hyperpolarization could not be reversed by passing hyperpolarizing current, but actually increased in size with higher membrane potentials. The minimum latency of the effect of acetylcholine or alpha-adrenergic agonists was 200-500 msec. Excitation of beta-adrenoceptors caused, after a long latency of several seconds, a small depolarization. Epinephrine induced a combined alpha- and beta-adrenergic response, with the alpha-component predominating. Blocking the alpha-adrenoceptors with phentolamine revealed the beta-adrenergic depolarization, while blocking the beta-adrenoceptors with propranolol caused the components of the alpha-adrenergic response to become more pronounced. All three receptors (alpha- and beta-adrenoceptors and cholinergic receptors) were present in individual acini.

Acetylcholine↗
PubMed1978

Antidiuresis induced by beta1- and beta2-adrenergic agonists in ethanol-anesthetized rats.

The beta1- and beta2-components in antidiuresis and sodium retention induced by beta-adrenergic agonists were analysed in ethanol-anesthetized, water-diuretic rats. Intravenous infusions of isoprenaline, salbutamol and carbuterol did not affect insulin clearance but increased plasma renin concentration to the same same extent. Propranolol completely blocked the decreases in urine volume (V) and urinary sodium excretion (UNaV) induced by isoprenaline; practolol (beta1-blocker) inhibited only the decrease in UNaV and butaxamine (beta2-blocker) inhibited only the decrease in V. The ratios of doses of beta-agonists which decreased UNaV and by 50% (ED50 UNaV decrease/ED50 V decrease) were 0.34, 0.68, 1.56 and 2.36 for isoprenaline, tretoquinol, salbutamol and carbuterol, respectively. This increasing order of the ratios coincided with the order reported for the preponderance of the beta2- over beta1-component of these agonists. These results indicate that the decrease in UNaV induced by beta-agonists is related to beta1 stimulation, while the decrease in V is related to beta2 stimulation.

Adrenergic beta-Agonists↗
PubMed1979

Airway response to adrenergic agonists and antagonists in 3-day- to 2-year-old rats.

The response of the airways to adrenergic agonists and antagonists was studied in 3-day- to 2-year-old and bronchitic rats. The results showed that the alpha-adrenoceptors are not functional at birth but become so by 8 weeks. In contrast, the beta-adrenoceptor effects are demonstrable on the third day after birth. The mean decrease in airway luminal diameter after beta-adrenergic blockade was greater in bronchitic than in healthy animals and was interpreted to be due to the increased sensitivity of the beta-adrenoceptors in bronchitis.

Acetylcholine↗
PubMed1976

Desensitization of beta-adrenergic receptors by beta-adrenergic agonists in a cell-free system: resensitization by guanosine 5'-(beta, gamma-imino)triphosphate and other purine nucleotides.

Incubation of purified frog erythrocyte membranes with beta-adrenergic agonists at 25 degrees produces relatively rapid (half-time about 10 min) desensitization (inactivation) of about 60% of the beta-adrenergic receptor binding sites. The desensitized receptors no longer bind the specific beta-adrenergic ligand (-)[3H]dihydroalprenolol. The decrease in the number of functional beta-adrenergic receptors is also manifest as a decreased ability of isoproterenol to stimulate the membrane-bound adenylate cyclase.

Adenylyl Cyclases↗
PubMed1976

Stimulation of glycogenolysis by beta adrenergic agonists in skeletal muscle of mice with the phosphorylase kinase deficiency mutation (I strain).

The mechanism by which beta adrenergic agonist stimulate glycogenolysis in intact skeletal muscle was investigated in mice with the phosphorylase kinase deficiency mutation (I strain). Although extracts of I strain diaphragm muscle had only 3.7% of the phosphorylase kinase activity found in extracts of the control strain (C57BL), incubation of I strain hemidiaphragms in Krebs-Ringer bicarbonate buffer with either isoproterenol or epinephrine resulted in a stimulation of the rate of glycogenolysis. In C57BL diaphragms, the EC50 values for isoproterenol and epinephrine were 2 and 14 nM, respectively. With I strain diaphragms, dl-isoproterenol or l-epinephrine stimulated glycogenolysis as a linear function of the log of the drug concentration with no apparent plateau of response up to concentrations of 30 to 40 mugM. For each 10-fold increase in drug concentration, isoproterenol and epinephrine stimulated glycogenolysis in I strain muscles an additional 0.37 to 0.42 mg/g/hr, a slope in the concentration-response relationship of 0.17 and 0.37, respectively, of that measured in C57BL diaphragms at concentrations around the EC50. The highest glycogenolytic response measured in I strain hemidiaphragms (at 40 mugM isoproterenol) was 80% of the maximal catecholamine-stimulated glycogenolysis in C57BL diaphragms. Both 4 nM and 4 mugM isoproterenol, in a concentration-dependent manner, stimulated phosphorylase b to a conversion in I and C57BL diaphragms and increased cyclic adenosine 3':5'-monophosphate (cyclic AMP) concentrations. The glycogenolytic response to 10.1 nM dl-isoproterenol in both I and C57BL diaphragms was blocked by 34 nM l-propranolol but not by 34 nM d-propranolol. The response to 4 mugM isoproterenol was enhanced by the cyclic nucleotide phosphodiesterase inhibitors papaverine (27 mugM) or dl-4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone (Ro 20-1724, 3 mugM). From the results of these studies, we conclude: 1) Catecholamines stimulate glycogenolysis in skeletal muscle of I mice, as in C57BL mice, by interacting with the beta adrenergic receptor, thereby increasing tissue cyclic AMP concentrations and stimulating phosphorylase b to a conversion. 2) alternative hypotheses for the mechanism of the catecholamine-stimulated decrease in glycogen concentration in I skeletal muscle-inhibition of glycogen synthesis, hyposia and 5'-AMP stimulation of phosphorylase b activity-have been ruled out. 3) the activity of the mutant phosphorylase kinase, although it is only 3.7% of that in extracts of C57BL muscle, is sufficient to produce phosphorylase b to a conversion and thereby account for the glycogenolytic response of I strain muscle to catecholamines.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗