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PubMed1984

Endothelial cells contain beta adrenoceptors.

The direct identification of beta adrenoceptors in endothelial cell cultures has not been possible until the advent of a new beta-adrenergic radioligand, [125I]iodocyanopindolol ([125I]ICYP). Using [125I]ICYP, we report the successful identification of a beta adrenoceptor in cultured bovine aortic endothelial cells. At 37 degrees C, specific binding is saturable, stable and reversible. There is a single class of binding sites (21,500 +/- 2,900 sites/cell) with an equilibrium dissociation constant (Kd) of 109 +/- 26 pM. The rate constant of association, k1, is 1.22 X 10(9) M-1 min-1 and of dissociation, k-1, is 0.01 min-1. Binding studies on monolayers of endothelial cells grown in microtiter plates yield similar data (Kd = 53 +/- 9 pM, Bmax = 20,000 +/- 1,900 sites/cell). Stereoselectivity of binding for the (-)-isomer is demonstrable for both agonists and antagonists. A series of adrenergic agonists competes with [125I]ICYP for binding with an order of potency suggesting beta 2 subselectivity ; isoproterenol (0.73 microM) greater than epinephrine (15 microM) greater than norepinephrine (71 microM). Furthermore, the beta 2 inhibitor butoxamine is more potent than the beta 1 inhibitor practolol (7.7 microM vs 22 microM respectively). The GTP analogue, Gpp(NH)p, reduces isoproterenol affinity to 1.9 microM and increases the Hill coefficient from 0.62-0.90.

Adrenergic beta-Agonists↗

PubMed1986

Effects of antiarrhythmic drugs on the extraneuronal accumulation of isoprenaline in perfused rat hearts.

The effects of class I, II, III and IV antiarrhythmic drugs (as classified by Vaughan Williams 1974), tetrodotoxin and beta 2-adrenoceptor antagonists on the extraneuronal accumulation of isoprenaline were examined in isolated rat hearts perfused with 3H-isoprenaline (1 mumol/l) and tropolone (100 mumol/l) for 30 min at a constant flow rate (6.5 ml/min) at 40 degrees C. Quinidine (class I), verapamil (IV), diltiazem (IV), dilazep (IV), nifedipine (IV), tetrodotoxin and butoxamine, at a concentration of 10 mumol/l, significantly decreased the extraneuronal accumulation of isoprenaline. The present study demonstrated that quinidine (class I) and all of the calcium channel blockers (class IV) had potent inhibitory effects on the extraneuronal accumulation of isoprenaline. The concentrations of these drugs needed for this decrease were nearly comparable to those needed to suppress isoprenaline-tropolone-induced ventricular fibrillation (Sono et al. 1985a). The antiarrhythmic effects of quinidine and calcium channel blockers in this experimental model may be partly due to a decrease in the extraneuronal accumulation of isoprenaline.

Adrenergic beta-Antagonists↗

PubMed1992

Adrenergic receptors coupled to adenylate cyclase in human cerebromicrovascular endothelium.

Cultured endothelium derived from three microvascular fractions of human brain was used to characterize adrenergic receptors coupled to adenylate cyclase activity. Catecholamines (norepinephrine, epinephrine) and their analogs (isoproterenol, phenylephrine, 6-fluoronorepinephrine) dose-dependently stimulated endothelial production of cAMP. Antagonists for beta 1 and beta 2 receptors (propranolol, atenolol, and butoxamine) and for alpha 1-receptors (prazosin) dose-dependently blocked cAMP formation induced by the tested adrenergic agonists. Clonidine, an alpha 2 > alpha 1-agonist, also inhibited isoproterenol-stimulated production of cAMP while yohimbine (alpha 2 > alpha 1 antagonist) augmented the norepinephrine or epinephrine-induced accumulation of cAMP. Cholera toxin-induced ADP ribosylation of the stimulatory guanine nucleotide binding protein (Gs) abolished the stimulatory effect of norepinephrine, epinephrine, phenylephrine or 6-fluoronorepinephrine on cAMP formation. ADP ribosylation of the inhibitory guanine nucleotide binding protein (Gi) by pertussis toxin had no effect on either phenylephrine- or 6-fluoronorepinephrine-induced production of cAMP while it increased the norepinephrine and epinephrine-induced accumulation of cAMP. These findings represent the first documentation of beta 1-, beta 2-, alpha 1 and alpha 2-adrenergic receptors linked to adenylate cyclase in endothelium derived from human brain microvasculature. These data also indicate that activation of endothelial alpha 1 -adrenergic receptors is mediated by a signal transduction mechanism associated with Gs protein. The results strongly support the presence of various receptor-controlled adrenergic regulatory mechanisms on human cerebromicrovascular endothelium.

Adenylyl Cyclases↗

PubMed1977

[The effect of sympathomimetric drugs on exocrine pancreatic function. Studies in the isolated cat pancreas (author's transl)].

This study reports on effects of beta-sympathomimetic drugs on the exocrine function of the isolated cat pancreas. The injection of these drugs resulted in an increase of pancreatic protein and enzyme secretion, the excretion of calcium into the juice and the rate of volume output were not changed. The enzyme secretion was inhibited by different adrenolytic drugs (phenoxybenzamine, practolol, butoxamine), by tetracain, hemicholinium, and atropine. The pancreatic function of cats pretreated by reserpine or 6-hydroxydopamine was not altered. It is concluded, that beta-sympathomimetic drugs influence the pancreatic protein and enzyme secretion in a cholinergic way. These results are consistent with those of other investigators showing a suppressibility of the isoproterenol-induced pancreatic amylase secretion by atropine.

Acetylcholine↗

PubMed1982

Rat serum stimulates serotonin N-acetyltransferase activity in pineal monolayer cultures.

The effects of rat serum on serotonin N-acetyltransferase (NAT) activity and indole synthesis in monolayer cultures of neonatal rat pineal glands was examined. The addition of 5% rat serum to these cultures resulted in stimulation of NAT activity equal to that obtained with optimal concentrations of the adrenergic agonist norepinephrine (NE). Rat serum also increased the synthesis of both N-acetylserotonin and melatonin from tryptophan. Stimulation of NAT activity by rat serum was partially blocked by metoprolol and propranolol, but not by phentolamine or butoxamine. The serum factor responsible for the stimulation was stable to both freezing and boiling. No significant amounts of epinephrine, norepinephrine, or dopamine were detected in the serum.

Acetyltransferases↗

PubMed2000

Oral beta-stimulants can inhibit passive cutaneous anaphylaxis in rats through an indirect inhibitory mechanism: possible involvement of afferent and efferent nervous system via gastric beta2-adrenoceptor stimulation.

OBJECTIVE AND DESIGN: We previously demonstrated that oral l-ephedrine exerts an extremely rapid (within 20 s) inhibition of 48-h passive cutaneous anaphylaxis reaction (PCA) in rats by a possibly unidentified mode of action. In the present experiments, we elucidated the mechanism of the PCA inhibition by l-ephedrine using adrenoceptor agonists and antagonists. MATERIALS: Rat antiserum was prepared with dinitrophenylated Ascaris suum extract + Bordetella pertussis. TREATMENT: Passively skin-sensitised Wistar rats were mainly used. l-Ephedrine, and adrenoceptor agonists and antagonists were orally administered immediately before PCA provocation. Catecholamine depleting (6-hydroxydopamine, 6-OHDA), amine depleting (reserpine) or ganglion blocking (hexamethonium) agent was intraperitoneally or intravenously administered before the provocation. METHODS: The effects of the drugs on PCA were assessed by inhibition of the dye leakage. RESULTS: beta-(propranolol) and beta2-(butoxamine) blocking agents reduced the inhibition of PCA by l-ephedrine, while the inhibition was not altered by either an a-blocking agent (phentolamine) or a beta1-(atenolol) selective antagonist. On the other hand, beta-(isoproterenol) and beta2-selective (salbutamol) agonists showed extremely rapid inhibition of PCA. However, the beta-selective agonist (dobutamine) had no effect on the reaction. The pretreatment with hexamethonium, reserpine or 6-OH-DA substantially attenuated the inhibitory effect of l-ephedrine on PCA. CONCLUSIONS: The results strongly suggest that beta2-adrenoceptors locate in the stomach and that their receptor excitement finally may lead to the inhibition of PCA via the stimulation of the central and peripheral nervous systems.

Adrenergic beta-2 Receptor Agonists↗

PubMed1986

Effects of electrical stimulation of the sympathetic nerve on the levels of beta-adrenergic and cholinergic muscarinic receptors and cyclic nucleotides in rat salivary glands.

After 30 and 60 min of stimulation, there were decrease of 16 to 19 per cent in beta-adrenoceptors in rat submandibular and parotid glands; a 10-min stimulation caused no change. Pre-incubation of the reaction mixtures (stimulated glands) with atenolol, a beta 1-antagonist, prevented most dihydroalprenolol (DHP) binding, but with butoxamine, a beta 2-antagonist, DHP binding was nearly complete. Thus the beta-receptor was of the beta 1-subtype. Muscarinic receptors of parotid gland showed no change after 10 min stimulation; after 30 min there was an increase of 12 per cent, and after 60 min, of 28 per cent. With submandibular gland, there was also no change at 10 min but, at 30 min, there was a 25 per cent increase, and at 60 min, a decrease of 18 per cent. Cyclic-AMP levels of parotid gland were markedly elevated after 10 min of stimulation (9-fold increase above controls) but, at 30 and 60 min, there was only a 1.6-fold increase. In submandibular gland, cyclic-AMP increased 10-fold at 10 min; at 30 min it was 2.5 times control levels and at 60 min, 1.9 times. Cyclic-GMP levels of parotid gland increased 34-fold after 30 or 60 min of nerve stimulation, but only 1.6-fold at 10 min. With submandibular gland, there was a 22-fold increase at 10 min, but at 30 and 60 min this was 15- and 12-fold, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1978

Dual effect of adrenalin on sugar transport in rat diaphragm muscle.

The effect of adrenalin on the membrane transport of the non-metabolized sugar, 3-methylglucose, was studied in isolated "intact" rat hemidiaphragms and related to simultaneously occurring changes in the internal levels of Na+, ATP, glucose-6-P, glycerol formation and 45Ca uptake and loss. Basal sugar transport was inhibited by low (10-8-10-5 M) concentrations of adrenalin; this was antagonized by propranolol and practolol. High concentrations (10-4-10-3 M) stimulated sugar transport, and this was blocked by propranolol and butoxamine and was dependent on external Ca2+. These results suggest interaction with two different classes of adrenergic receptors, possibly of beta 1 and beta 2 types. Both low and high concentrations increases Na+ and K+ gradients by a practolol-sensitive effect. Isoproterenol behaved identically but phenylephrine had only the two practolol-sensitive effects on sugar and ion transport. Insulin did not interfere with inhibition of sugar transport and decrease in internal Na+ but prevented stimulation of sugar transport. Under anoxia adrenalin had no effect on sugar transport but led to greater Na+ gain by tissue. Addition of 3.0 mM palmitate decreased inhibition of sugar transport without changing receptor specificity. ATP was decreased and lipolysis enchanged by high adrenalin but glucose-6-P was increased by the low concentration as well. Influx of 45 Ca was decreased by low and increased by high adrenalin; 45Ca efflux was also differentially affected. The results indicate that inhibition and stimulation of sugar transport depend on different receptors and that the latter response may override the former. The data are consistent with the earlier postulated regulatory role of sarcoplasmic Ca2+ on sugar transport in muscle, with adrenalin affecting Ca2+ fluxes and distribution both directly and indirectly.

Animals↗

PubMed1987

Coordinate increases and decreases in mitochondrial RNA and ATP syntheses produced by propranolol and rifampicin.

A variety of compounds were examined for their capacity to alter RNA synthesis in isolated rat cardiac and hepatic mitochondria. The beta-adrenergic blocking agents propranolol and butoxamine, and the antiarrhythmic agent quinidine, produced a concentration-dependent stimulation of RNA synthesis in cardiac and hepatic mitochondria. In contrast, the antitubercular antibiotic rifampicin produced a concentration-dependent inhibition of RNA synthesis in cardiac and hepatic mitochondria. Propranolol, as a representative compound which stimulated RNA synthesis, was also found to stimulate ATP synthesis in isolated mitochondria, whereas rifampicin inhibited ATP synthesis. Coordinate increases and decreases in RNA and ATP syntheses suggest that agents which stimulate or inhibit RNA synthesis may rapidly alter ATP synthesis. This finding is consistent with the rapid turn-over of mitochondrial RNA with a messenger function (1.4 and 3.3 min in isolated rat cardiac and hepatic mitochondria), and it suggests that mitochondrial RNA must continue to be synthesized to maintain inner membrane systems required for ATP synthesis. Stimulation of RNA and ATP syntheses by propranolol through membrane stabilization or other actions represents a heretofore unrecognized action of propranolol which may contribute to its beneficial therapeutic effects.

Adenosine Triphosphate↗

PubMed1989

Identification of functional beta-adrenergic receptors on AC glioma cells.

AC glioma cells, a clonal cell line derived from a rat glioma, responded to 1 mM dibutyryl-cyclic AMP and isobutylmethylxanthine with a change to stellate morphology. A concentration-related morphological change was induced by beta 1- and beta 2-adrenergic agonists with the order of potency being isoproterenol greater than soterenol greater than norepinephrine. Propranolol (nonselective, beta-antagonist), butoxamine (beta 2-antagonist) and metoprolol (beta 1-antagonist) significantly decreased the cell response to isoproternol. Schild analysis of the response, using the competitive antagonist metoprolol, gave pA2 values of 7.5 and 8.5 for the agonists norepinephrine and soterenol, respectively, with slopes of the curves being less than unity. These observations indicate that both beta 1- and beta 2-adrenergic receptors mediate the change in cellular morphology.

Animals↗

PubMed1979

The resolution of dopamine and beta 1- and beta 2-adrenergic-sensitive adenylate cyclase activities in homogenates of cat cerebellum, hippocampus and cerebral cortex.

The stimulation of adenylate cyclase by dopamine and various beta-adrenergic agonists has been investigated in homogenates from 3 areas of cat brain: the cerebral cortex, cerebellum and hippocampus. The purpose of the study was to determine whether the beta-arenergic receptors coupled to adenylate cyclase could be classified as either beta 1 and beta 2 subtypes in the different regions studied. The stimulation of adenylate cyclase by the beta-adrenergic agonist, (-)isoproterenol (5 X 10(-6) M), was completely blocked by the specific beta-adrenergic antagonist, (p)alprenolol (1-(-5) M), but not by the dopaminergic antagonist, fluphenazine (10(-5) M), whereas the stimulation of adenylate cyclase by (-)epinephrine (10(-4) M) was blocked to varying extents by these two drugs in each of the 3 regions studied. The (-)epinephrine effect was always blocked in the combined presence of (p)alprenolol and fluphenazine. The adenylate cyclase stimulation by (p)epinephrine which is not blocked by (p)alprenolol was due to interaction of (p)epinephrine with a dopaminergic-sensitive adenylate cyclase which has been characterized in cerebral cortex, hippocampus and cerebellum. Regional differences in the affinity of beta-adrenergic-sensitive adenylate cyclase for various agonists were investigated in the presence of fluphenazine (10(-5) M). In the cerebellum the potency order was (+/-)protokylol greater than (+/-)hydroxybenzylisoproterenol greater than (+/-)isoproterenol greater than (-)epinephrine greater than (+/-)salbutamol greater than (-)norepinephrine, indicating the presence of a beta 2-adrenergic receptor. In the cerebral cortex the potency order was (-)isoproterenol greater than +/-)protokylol greater than (+/-)hydroxybenzylisoproterenol greater than (-)epinephrine = (-)norepinephrine ((+/-)salbutamol being inactive). A similar pattern was found in the hippocampus indicating the presence of a beta 1-adrenergic receptor in these two regions. (+/-)Salbutamol was a partial agonist in the cerebellum and a competitive antagonist in the cerebral cortex. The ratio of the antagonist potencies of (+/-)practolol and (+/-)butoxamine preferential beta 1- and beta 2-adrenergic antagonists respectively, to block the stimulation of adenylate cyclase was 25 in the cerebellum, compared to 0.5 in the cerebral cortex and 1.6 in the hippocampus. These results confirm the presence of a beta 2 subtype of receptor coupled to adenylate cyclase in the former and beta 1 subtypes in the latter two regions. The comparison between the affinities of a series of beta-adrenergic agonists and antagonists for the beta-adrenergic receptors coupled with an adenylate cyclase in cerebral cortex and cerebellum with their affinities for well characterized beta 2-adrenergic receptors in lung and beta 1-adrenergic receptor in heart substantiated this conclusion.

Adenylyl Cyclases↗

PubMed1991

High-dose epinephrine acts at alpha 2-adrenoceptors to suppress experimental arthritis.

This study assessed the receptor site at which high systemic doses of epinephrine act to reduce the severity of adjuvant-induced arthritis in the rat. To this end we examined the effect of selective adrenergic antagonists on the reduction of arthritis by epinephrine, and also assessed whether high doses of selective adrenergic agonists mimicked the effect of epinephrine. The decrease in arthritis induced by epinephrine (0.5 mg/kg in chronic implant injected every 3 days) was significantly antagonized by the selective alpha 2-adrenergic antagonist, yohimbine, but not by selective alpha 1 (prazosin), beta 1 (metoprolol) or beta 2 (butoxamine) antagonists. In addition, chronic infusion of the alpha 2-adrenergic agonist clonidine, but not selective alpha 1 (phenylephrine), beta 1/beta 2 (isoproterenol) or beta 2 (salbutamol) agonists, resulted in decreased arthritis severity. These data suggest that the suppressive effect of high-dose epinephrine on joint injury in experimental arthritis is mediated by action at the alpha 2-adrenergic receptor.

Adrenergic alpha-Agonists↗

PubMed1994

Effect of neurotransmitters on axoplasmic transport: how adrenaline affects superior cervical ganglion cells.

The effect of adrenaline on the axoplasmic transport of cultured superior cervical ganglion cells was analyzed with a computer-assisted video-enhanced differential interference contrast microscope system. Adrenaline increased the axoplasmic transport reversibly in both anterograde and retrograde directions. A beta 2-antagonist, butoxamine, antagonized the increasing effects of adrenaline, but alpha-antagonists and beta 1-antagonists did not. A beta 2-agonist, albuterol, mimicked the adrenaline effect, but beta 1-, alpha 1-, alpha 2-agonists did not. The adrenaline receptor may be a beta 2-receptor. Dibutyryl cyclic AMP and forskolin increased the axoplasmic transport. Therefore, adrenaline increases the axoplasmic transport by raising the cyclic AMP level. In light of our former report that acetylcholine suppresses the axoplasmic transport, neurotransmitters control axoplasmic transport and this neurotransmitter control reflects the activity of the nerve cell.

Albuterol↗

PubMed1976

Inhibition by alpha- and beta-adrenoceptors of the twitch response to transmural stimulation in the guinea-pig vas deferens.

Noradrenaline as well as the indirectly acting amines tyramine and phenethylamine either enhance or inhibit the twitch response of the transmurally stimulated, isolated guine-pig vas deferens, thus partly confirming previous reports. In both cases enhancement is annulled by alpha-adrenoceptor blockers. The twitch inhibition caused by noradrenaline is abolished by alpha- + beta2-adrenoceptor blockers, but not by either blocker alone. The inhibition caused by the indirectly acting amines is largely abolished by alpha-adrenoceptor blockers. Clonidine strongly inhibits the twitch. This effect if promptly removed by phentolamine. After blockade of the neurally induced twitch by tetrodotoxin, noradrenaline and the indirectly acting amines have no effect or slightly enhance the twitch elicited by transmural stimulation of the smooth muscle. It is concluded that exogenous noradrenaline acts on postjunctional stimulatory alpha-adrenoceptors and on inhibitory alpha- and beta2-adrenoceptors, which are presumably prejunctional. In the unstimulated preparation contracted by acetylcholine, noradrenaline causes further contraction which is changed into relaxation after phentolamine. This relaxation is abolished by butoxamine, suggesting that noradrenaline may also act on inhibitory postjunctional beta2-adrenoceptors. The twitch-inhibiting effect of endogenous noradrenaline, released by nerve stimulation or by indirectly acting amines, appears to be primarily mediated by prejunctional alpha-adrenoceptors.

Animals↗

PubMed1978

Beta-adrenoceptors modulate noradrenaline release from axonal sprouts in cultured rat superior cervical ganglia.

Superior cervical ganglia of rats grown in organ culture were used to study the effect of beta-receptor stimulants and antagonists on 3H-noradrenaline release in response to stimulation by KC1 (75 mM). (--)-Isoprenaline 1X 10(-9)--1 X 10(-7) M) increased 20--25% the release of 3H-noradrenaline from cultured ganglia exposed to KC1. Isoprenaline did not modify either the spontaneous (non-calcium dependent) release of 3H-noradrenaline from cultured ganglia, or the KC1-stimulated release from fresh ganglia. The effect of (--)-isoprenaline was blocked by (--)-propranolol 5 X 10(-9) -- 1 X 10(-8) M and by butoxamine 10(-6) M, but not by (+)-propranolol (1 -- 5 X 10(-8) M), practolol (1 X 10(-8) -- 1 X 10(-6) M), or sotalol (1 X 10(-7) -- 1 X 10(-6) M). Isoprenaline induced augmentation of 3H-noradrenaline release and its antagonism by (--)-propranolol still occurred in the presence of DMI. It is suggested that presynaptic beta-receptors in sympathetic nerve terminals may be involved in a positive feedback of noradrenaline release.

Adrenergic beta-Antagonists↗

PubMed1979

Alterations in blood levels of carbohydrate and lipid metabolites and of cyclic AMP mediated by beta1- and beta2-adrenoceptors in beagle dogs: effects of procaterol, a new selective beta2-adrenoceptor agonist.

The intravenous injection of isoprenaline (10 nmole/kg) into conscious beagle dogs caused significant increases in the blood level of lactate, glucose, FFA, insulin and cyclic AMP. These metabolic alterations induced by isoprenaline were blocked completely by pretreatment of the dog with propranolol (1 mg/kg). Butoxamine (10 mg/kg) antagonized isoprenaline-induced increases in glucose, lactate and insulin, but not the increases in FFA. Practolol (10 mg/kg) diminished the increase in blood FFA very strongly. Salbutamol, which is known to be an agonist of the beta 2-subtype in its bronchomotor and cardiovascular actions, produced marked increases in the blood concentrations of lactate, glucose and insulin but were without effect on the FFA level. Thus metabolic responses of conscious beagle dogs to beta-adrenoceptor agonists appeared to depend differentially on two types of beta-adrenoceptors: beta1-adrenoceptors are largely involved in lipolysis while beta2-adrenoceptors are involved in the regulation of blood glucose metabolism and insulin secretion. A new beta-adrenoceptor agonist, 5-(1-hydroxy-2-isopropylaminobutyl)-8-hydroxycarbostyril hydrochloride hemihydrate (Procaterol), was classified as a beta 2-agonist, because it markedly increased plasma concentrations of glucose, lactate and insulin but increased the plasma level of FFA to a lesser degree. The order of potency of beta2-agonists was procaterol greater than salbutamol greater than trimetoquinol. Metabolic responses of beagle dogs would be useful for appreciating the selectivity and potency of beta-adrenoceptor agonists and antagonists.

Adrenergic beta-Agonists↗

PubMed1982

Specificity of the beta 2-adrenergic receptor stimulating cyclic AMP accumulation in the intermediate lobe of rat pituitary gland.

Changes of cyclic AMP levels were used to assess the specificity of the beta-adrenergic receptor in primary cultures of cells prepared from the intermediate lobe of rat pituitary gland. During a 4 min incubation, beta-adrenergic agonists led to a 4 to 6 fold stimulation of cyclic AMP concentration with the following order of potency (Kd values): zinterol (0.75 nM) greater than hydroxybenzylisoproterenol (1.0 nM) greater than (--)-isoproterenol (4.6 nM) greater than soterenol greater than (7.7 nM) greater than (--)-epinephrine (10 nM) greater than OPC 2009 (procaterol, 11 nM) much greater than (--)-norepinephrine (300 nM). The potent antagonists cyanopindolol, (--)-propranolol and hydroxybenzylpindolol reversed the stimulatory effect of (--)-isoproterenol at Kd values of 0.4-0.6 nM. Other beta-adrenergic antagonists had the following order of potency: pindolol = (--)-alprenolol = timolol (0.9-1.0 mM) much greater than metoprolol (100 nM) greater than dichloroisoproterenol (300 nM) greater than butoxamine (1100 nM). The beta 1-selective antagonist practolol had a low potency at 700 nM. The stereoselectivity of the receptor is indicated by the 400 to 70 fold higher potency of the (--)-isomers of isoproterenol, epinephrine and propranolol as compared to their (+)-stereoisomers. The data show that the beta-adrenergic receptor in the intermediate lobe of the rat pituitary gland is mainly of the bet 2-subtype. Study of this pure population of postsynaptic beta-adrenergic receptors where binding could be correlated with other parameters of cellular activity (cyclic AMP formation and alpha-MSH secretion) should yield useful information about the less accessible adrenergic systems of the brain.

Animals↗

PubMed1983

Further characterization of presynaptic beta-adrenoceptors in guinea-pig pulmonary arteries.

Presynaptic beta-adrenoceptors were further characterized in spiral strips of guinea-pig pulmonary arteries preloaded with [3H]norepinephrine. l-Metoprolol (3 X 10(-6) M) inhibited isoproterenol (3 X 10(-7) M)-induced increases in 3H efflux by transmural field stimulation, whereas the d-isomer produced no inhibition. However, IPS 339, H 35/25, butoxamine and metoprolol (3 X 10(-6) M) antagonized salbutamol (3 X 10(-7) M)-induced increases in the parameter, whereas acebutolol, bevantolol and practolol (3 X 10(-6) M) produced no antagonism. Presynaptic beta-adrenoceptors in guinea-pig pulmonary arteries appear to have characteristics similar to those postsynaptic classical beta-adrenoceptors.

Albuterol↗