brl-37344 and amibegron

brl-37344 has been researched along with amibegron* in 12 studies

Other Studies

12 other study(ies) available for brl-37344 and amibegron

ArticleYear
β
    Journal of neurophysiology, 2019, 03-01, Volume: 121, Issue:3

    Action potential firing in hippocampal pyramidal neurons is regulated by generation of an afterhyperpolarization (AHP). Three phases of AHP are recognized, with the fast AHP regulating action potential firing at the onset of a burst and the medium and slow AHPs supressing action potential firing over hundreds of milliseconds and seconds, respectively. Activation of β-adrenergic receptors suppresses the slow AHP by a protein kinase A-dependent pathway. However, little is known regarding modulation of the medium AHP. Application of the selective β-adrenergic receptor agonist isoproterenol suppressed both the medium and slow AHPs evoked in rat CA1 hippocampal pyramidal neurons recorded from slices maintained in organotypic culture. Suppression of the slow AHP was mimicked by intracellular application of cAMP, with the suppression of the medium AHP by isoproterenol still being evident in cAMP-dialyzed cells. Suppression of both the medium and slow AHPs was antagonized by the β-adrenergic receptor antagonist propranolol. The effect of isoproterenol to suppress the medium AHP was mimicked by two β

    Topics: Adrenergic beta-Agonists; Animals; CA1 Region, Hippocampal; Cyclic AMP; Ethanolamines; Isoproterenol; Male; Membrane Potentials; Potassium Channel Blockers; Pyramidal Cells; Pyrimidines; Rats; Rats, Wistar; Receptors, Adrenergic, beta; Small-Conductance Calcium-Activated Potassium Channels; Tetrahydronaphthalenes

2019
Behavioral and neurophysiological evidence that lateral paracapsular GABAergic synapses in the basolateral amygdala contribute to the acquisition and extinction of fear learning.
    Neurobiology of learning and memory, 2016, Volume: 127

    The lateral/basolateral amygdala (BLA) is crucial to the acquisition and extinction of Pavlovian fear conditioning, and synaptic plasticity in this region is considered to be a neural correlate of learned fear. We recently reported that activation of BLA β3-adrenoreceptors (β3-ARs) selectively enhances lateral paracapsular (LPC) feed-forward GABAergic inhibition onto BLA pyramidal neurons, and that intra-BLA infusion of a β3-AR agonist reduces measures of unconditioned anxiety-like behavior. Here, we utilized a combination of behavioral and electrophysiological approaches to characterize the role of BLA LPCs in the acquisition of fear and extinction learning in adult male Long-Evans rats. We report that intra-BLA microinjection of β3-AR agonists (BRL37344 or SR58611A, 1μg/0.5μL/side) prior to training fear conditioning or extinction blocks the expression of these behaviors 24h later. Furthermore,ex vivo low-frequency stimulation of the external capsule (LFS; 1Hz, 15min), which engages LPC synapses, induces LTP of BLA fEPSPs, while application of a β3-AR agonist (SR58611A, 5μM) induces LTD of fEPSPs when combined with LFS. Interestingly, fEPSP LTP is not observed in recordings from fear conditioned animals, suggesting that fear learning may engage the same mechanisms that induce synaptic plasticity at this input. In support of this, we find that LFS produces LTD of inhibitory postsynaptic currents (iLTD) at LPC GABAergic synapses, and that this effect is also absent following fear conditioning. Taken together, these data provide preliminary evidence that modulation of LPC GABAergic synapses can influence the acquisition and extinction of fear learning and related synaptic plasticity in the BLA.

    Topics: Adrenergic beta-Agonists; Animals; Basolateral Nuclear Complex; Conditioning, Classical; Electric Stimulation; Ethanolamines; External Capsule; Extinction, Psychological; Fear; GABAergic Neurons; Male; Neuronal Plasticity; Pyramidal Cells; Rats; Rats, Long-Evans; Reflex, Startle; Synaptic Potentials; Tetrahydronaphthalenes

2016
Human atrial β(1L)-adrenoceptor but not β₃-adrenoceptor activation increases force and Ca(2+) current at physiological temperature.
    British journal of pharmacology, 2011, Volume: 162, Issue:4

    It has been proposed that BRL37344, SR58611 and CGP12177 activate β₃-adrenoceptors in human atrium to increase contractility and L-type Ca(2+) current (I(Ca-L)). β₃-adrenoceptor agonists are potentially beneficial for the treatment of a variety of diseases but concomitant cardiostimulation would be potentially harmful. It has also been proposed that (-)-CGP12177 activates the low affinity binding site of the β₁-adrenoceptor in human atrium. We therefore used BRL37344, SR58611 and (-)-CGP12177 with selective β-adrenoceptor subtype antagonists to clarify cardiostimulant β-adrenoceptor subtypes in human atrium.. Human right atrium was obtained from patients without heart failure undergoing coronary artery bypass or valve surgery. Cardiomyocytes were prepared to test BRL37344, SR58611 and CGP12177 effects on I(Ca-L). Contractile effects were determined on right atrial trabeculae.. BRL37344 increased force which was antagonized by blockade of β₁- and β₂-adrenoceptors but not by blockade of β₃-adrenoceptors with β₃-adrenoceptor-selective L-748,337 (1 µM). The β₃-adrenoceptor agonist SR58611 (1 nM-10 µM) did not affect atrial force. BRL37344 and SR58611 did not increase I(Ca-L) at 37°C, but did at 24°C which was prevented by L-748,337. (-)-CGP12177 increased force and I(Ca-L) at both 24°C and 37°C which was prevented by (-)-bupranolol (1-10 µM), but not L-748,337.. We conclude that the inotropic responses to BRL37344 are mediated through β₁- and β₂-adrenoceptors. The inotropic and I(Ca-L) responses to (-)-CGP12177 are mediated through the low affinity site β(1L)-adrenoceptor of the β₁-adrenoceptor. β₃-adrenoceptor-mediated increases in I(Ca-L) are restricted to low temperatures. Human atrial β₃-adrenoceptors do not change contractility and I(Ca-L) at physiological temperature.

    Topics: Adrenergic beta-Agonists; Adrenergic beta-Antagonists; Aged; Atrial Appendage; Calcium Channels, L-Type; Calcium Signaling; Ethanolamines; Female; Humans; In Vitro Techniques; Kinetics; Male; Middle Aged; Myocardial Contraction; Myocytes, Cardiac; Propanolamines; Receptors, Adrenergic, beta-1; Receptors, Adrenergic, beta-2; Receptors, Adrenergic, beta-3; Temperature; Tetrahydronaphthalenes

2011
Involvement of beta1- and beta2- but not beta3-adrenoceptor activation in adrenergic PYY secretion from the isolated colon.
    The Journal of endocrinology, 2001, Volume: 168, Issue:1

    The secretion of PYY by endocrine L cells of the terminal gut is under the control of nutrients, the autonomic nervous system and hormones. Catecholamines, and the non-specific beta-adrenergic agonist isoproterenol induce PYY secretion from rat isolated colon or ileum. Because beta3-adrenergic receptors now appear to mediate many of the effects of catecholamines in the gastrointestinal tract, we investigated the involvement of beta1-, beta2-, and beta3-adrenoceptor stimulation in PYY secretion from the isolated, vascularly perfused rat colon. Infusion of 10(-6) M isoproterenol induced a transient increase in PYY secretion (from 36+/-4 to 87+/-20 fmol/2 min; n=7, P<0.05), that was abolished by a previous infusion of the beta1- and beta2-adrenergic blocker (and partial beta3-agonist) alprenolol (10(-6) M). The beta1-adrenergic agonist dobutamine and the beta-2 agonist terbutaline also (both at 10(-5) M) significantly stimulated PYY secretion, from 29+/-1 to 79+/-12 fmol/2 min and from 19+/-1 to 73+/-13 fmol/2 min respectively (n=7, P<0.05). Neither of the beta3-adrenergic agonists tested (BRL 37 344 (10(-5), 10(-6) M) and SR 58 611A (10(-6) M)) significantly stimulated PYY secretion, thus confirming the exclusive involvement of beta1- and beta2-receptors in beta-adrenergic agonist induced hormone secretion.

    Topics: Adrenergic beta-Agonists; Adrenergic beta-Antagonists; Alprenolol; Animals; Colon; Dobutamine; Ethanolamines; Isoproterenol; Male; Models, Animal; Organ Culture Techniques; Peptide YY; Rats; Rats, Wistar; Receptors, Adrenergic, beta; Receptors, Adrenergic, beta-1; Receptors, Adrenergic, beta-2; Receptors, Adrenergic, beta-3; Statistics, Nonparametric; Terbutaline; Tetrahydronaphthalenes

2001
Enhancement of memory consolidation in chicks by beta(3)-adrenoceptor agonists.
    European journal of pharmacology, 2001, Feb-16, Volume: 413, Issue:2-3

    The effects of intracranial injection of three beta(3)-adrenoceptor agonists, sodium-4-[-2[-2-hydroxy-2-(-3-chloro-phenyl)ethylamino] propyl]phenoxyacetate (BRL 37344), 2-hydroxy-5(2-((2-hydroxy-3-(4-((1-methyl-4-trifluoromethyl)1H-imidazole-2-yl)-phenoxy)propyl)amino)ethoxy)-benzamide monomethane sulfonate) (+/-)-CGP12177A) and the pro-drug RS-N-(7-carbethoxymethoxyl 1,2,3,4-tetrahydronaphth-2-yl)-2 hydroxy 2-(3-chlorophenyl)ethanamine (SR58611A), were examined on reinforcement of memory in day-old chicks. BRL37344 and CGP12177 facilitated memory, whereas SR58611A had no effect. The dose-response relationships of the beta(3)-adrenoceptor agonists were challenged with the selective beta(3)-adrenoceptor antagonist 3-(2-ethylphenoxy)-1-[(1S)-1,2,3,4-tetrahydronapth-1-ylamino]-2S-2-propanol oxalate (SR59230A) or the beta(2)-adrenoceptor antagonist (-)propranolol. BRL 37344 appeared to act predominantly at beta(3)-adrenoceptors at low doses and at beta(2)-adrenoceptors at higher doses. Facilitation of labile into long-term storage by beta(3)-adrenoceptor agonists appears to be a class action of these drugs.

    Topics: Adrenergic beta-Agonists; Adrenergic beta-Antagonists; Animals; Animals, Newborn; Avoidance Learning; Chickens; Discrimination Learning; Dose-Response Relationship, Drug; Ethanolamines; Female; Memory; Propanolamines; Propranolol; Receptors, Adrenergic, beta-3; Tetrahydronaphthalenes

2001
Phosphorylation of extracellular signal-regulated kinases 1 and 2 in 3T3-L1 adipocytes by stimulation of beta(3)-adrenoceptor.
    European journal of pharmacology, 1999, Nov-26, Volume: 385, Issue:1

    Recent studies have revealed that activated extracellular signal-regulated kinases (ERKs) 1 and 2 by the stimulation of beta(3)-adrenoceptors played a critical role in cell survival in brown adipocytes. On the other hand, phosphorylation of ERK1/2 via beta(3)-adrenoceptors and its physiological and pathological significance in white adipocyte has remained uncertain despite the increasing significance of functioning white adipocytes. Accordingly, we here studied phosphorylation of ERK1/2 caused by the stimulation of beta(3)-adrenoceptors in 3T3-L1 adipocytes, and the roles of phosphorylated ERK1/2 in lipolysis. Phosphorylation of ERK1/2 was induced by a selective beta(3)-adrenoceptor agonist, DL-4-[2'-¿2-hydroxy-2-(3-chlorophenyl)ethylamino¿propyl] phenoxyacetic acid sodium salt sesquihydrate (BRL37344), in 3T3-L1 adipocytes in a time- and dose-dependent manner. The phosphorylation of ERK1/2 by BRL37344 was sensitive to the cyclic AMP (cAMP)-dependent protein kinase inhibitor, N-[2-((p-bromocinnamyl)amino)ethyl]-5-isoquinolinesulfonamide (H89). To elucidate the roles of phosphorylated ERK1/2 in lipolysis, the effect of a selective inhibitor of ERK1/2 phosphorylation, 2'-amino-3'-methoxyflavone (PD98059), was examined. This inhibitor did not alter the lipolytic action caused by BRL37344, even at concentrations sufficient to block phosphorylation of ERK1/2, suggesting that ERK1/2 play no role in the lipolysis caused by BRL37344 in 3T3-L1 adipocytes.

    Topics: 3T3 Cells; Adipocytes; Adrenergic beta-Agonists; Adrenergic beta-Antagonists; Animals; Cyclic AMP-Dependent Protein Kinases; Dose-Response Relationship, Drug; Enzyme Inhibitors; Ethanolamines; Flavonoids; Glycerol; Isoquinolines; Mice; Mitogen-Activated Protein Kinases; Phosphorylation; Propanolamines; Propranolol; Receptors, Adrenergic, beta; Receptors, Adrenergic, beta-3; Sulfonamides; Tetrahydronaphthalenes

1999
Functional identification of rat atypical beta-adrenoceptors by the first beta 3-selective antagonists, aryloxypropanolaminotetralins.
    British journal of pharmacology, 1996, Volume: 117, Issue:3

    1. We have assessed the relative abilities of compounds belonging to the new aryloxypropanolaminotetralin (APAT) class and of the reference beta-adrenoceptor-blocking agent, alprenolol, to antagonize functional responses in vitro and in vivo involving atypical (beta 3) or conventional (beta 1 and beta 2) beta-adrenoceptors. 2. The range of pA2 values for three representative APATs against inhibition of spontaneous motility in the rat isolated colon by the selective beta 3-adrenoceptor agonist, SR 58611A (8.1-8.8), was well above similarly calculated values for non-competitive antagonism of guinea-pig trachea relaxation by salbutamol (beta 2, 6.5-6.9) and the atrial chronotropic response by isoprenaline (beta 1, 6.7-7.3). Alprenolol, however, was substantially more potent in antagonizing atrial (pA2, 8.2) and tracheal (pA2, 8.9) responses than SR 58611A mediated inhibition of colonic motility (pA2, 6.8). 3. Several APAT isomers with different configurations at the chiral carbons, when tested on isolated organs, presented stringent stereochemical requirements for beta 3-selectivity, including high antagonist potency-ratios between active and inactive enantiomers. 4. In vivo, the inhibition of colonic motility and the thermogenic response of brown adipose tissue elicited in rats by the selective beta 3-adrenoceptor agonists SR 58611A and BRL 37344 respectively were substantially diminished by the representative APAT, SR 59230A, at oral doses (< or = 5 mg kg-1) well below those half maximally effective (ID50) for preventing beta 1-(isoprenaline tachycardia > or = 80 mg kg-1) or beta 2-(salbutamol bronchodilatation, 44 mg kg-1) mediated responses. Alprenolol, as expected, was a less potent and nonselective antagonist of the putative beta 3-responses. 5. These findings support APATs as the first potent, orally effective selective antagonists at beta 3-adrenoceptors, and provide final unambiguous evidence that beta 3-adrenoceptors underlie inhibition of colonic motility and brown adipose tissue thermogenesis in rats.

    Topics: Adipose Tissue; Adrenergic beta-Agonists; Adrenergic beta-Antagonists; Airway Resistance; Alprenolol; Animals; Body Temperature Regulation; Colon; Ethanolamines; Gastrointestinal Motility; Guinea Pigs; Heart; Heart Rate; In Vitro Techniques; Male; Propanolamines; Rats; Receptors, Adrenergic, beta; Tetrahydronaphthalenes; Trachea

1996
Beta 3-adrenoceptor agonists, BRL 37344 and SR 58611A, do not induce relaxation of human, sheep and guinea-pig airway smooth muscle in vitro.
    The European respiratory journal, 1994, Volume: 7, Issue:9

    The existence of atypical- or beta 3-adrenoceptors has now been generally accepted. These receptors have been shown to be abundant in adipose tissue and in a number of gastrointestinal smooth muscle preparations. A recent study reported that beta 3-adrenoceptor stimulation mediated relaxation of isolated canine bronchial smooth muscle. The aim of the present study was to extend this observation to other species. We investigated the in vitro responses of guinea-pig, human and sheep bronchial smooth muscle to isoprenaline, salbutamol (a selective beta 2-adrenoceptor agonist), and BRL 37344 and SR 58611A (two presumably selective beta 3-adrenoceptor agonists). The preparations were precontracted to 60-70% of maximal tension with histamine 10(-6) M for guinea-pig and human bronchi, or acetylcholine 10(-6) M for sheep bronchi. In each species, SR 58611A produced a slight fall in tension of about 10% of the effects of theophylline (3 mM), but this decrease in tension was not significantly different from the spontaneous and weak relaxation observed with saline addition during the same duration of the experiment. These relaxations were not modified by either the nonselective beta-adrenoceptor antagonist propranolol or the selective beta 2-adrenoceptor antagonist ICI 118,551. In contrast, BRL 37344 induced a significant concentration-dependent fall in tension induced by both spasmogens. Its relaxant effects were inhibited both by propranolol and ICI 118,551 in human and guinea-pig airways, whereas on the isolated sheep bronchus BRL 37344-induced relaxations were only slightly, albeit significantly, reduced with either of the beta-adrenoceptor antagonists tested.(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: Adrenergic beta-Agonists; Animals; Bronchi; Ethanolamines; Female; Guinea Pigs; Humans; In Vitro Techniques; Male; Muscle Relaxation; Muscle, Smooth; Receptors, Adrenergic, beta; Receptors, Adrenergic, beta-3; Sheep; Stereoisomerism; Tetrahydronaphthalenes

1994
Similar atypical beta-adrenergic receptors mediate in vitro rat adipocyte lipolysis and colonic motility inhibition.
    Life sciences, 1993, Volume: 53, Issue:18

    We investigated the putative common nature of the rat atypical beta-adrenoceptors mediating white adipocyte lipolysis and proximal colon motility inhibition, using the non-selective antagonist alprenolol and agonist isoprenaline and the selective agonists SR 58611A and BRL 37344. Results in either isolated intestinal and fat tissues were consistent with: isoprenaline acting through both typical (beta 1, beta 2) and typical beta-adrenoceptors; SR 58611A and BRL 37344 acting solely through the latter. The identical pA2 values obtained with alprenolol, irrespective of the tissue and the selective agonist (SR 58611A or BRL 37344) used, support the high functional homology of the atypical beta-adrenoceptors in rat colon and adipocytes.

    Topics: Adipocytes; Adrenergic beta-Agonists; Alprenolol; Animals; Atrial Function; Colon; Ethanolamines; Gastrointestinal Motility; Guinea Pigs; Heart Atria; In Vitro Techniques; Isoproterenol; Lipolysis; Male; Rats; Receptors, Adrenergic, beta; Tetrahydronaphthalenes; Trachea

1993
Effects of two beta 3-adrenoceptor agonists, SR 58611A and BRL 37344, and of salbutamol on cholinergic and NANC neural contraction in guinea-pig main bronchi in vitro.
    British journal of pharmacology, 1993, Volume: 110, Issue:4

    1. The aim of the present study was to investigate the type of adrenoceptor which modulates constriction of the guinea-pig isolated main bronchus in response to electrical field stimulation (EFS). Drugs used were salbutamol and two agonists reportedly selective for the putative beta 3-adrenoceptor: BRL 37344 and SR 58611A. 2. At basal tone, all three drugs induced relaxation, however, SR 58611A and BRL 37344 (10(-9) to 10(-6) M) relaxed guinea-pig isolated main bronchus more weakly than salbutamol (10(-9) to 10(-6) M). The effects observed at 10(-6) M were 43% +/- 9%, 63% +/- 4% and 98% +/- 1% of the maximal effect induced by theophylline (3 x 10(-3) M) for SR 58611A, BRL 37344 and salbutamol, respectively. 3. SR 58611A and BRL 37344 (10(-8) to 10(-6) M) did not significantly modify the cholinergic component of the response to EFS, but caused a concentration-dependent reduction of the nonadrenergic non-cholinergic (NANC) excitatory component (41.8% +/- 10.1% and 56.8% +/- 7.4% respectively at 10(-6) M, n = 6-7). Salbutamol (10(-9) to 10(-7) M) strongly inhibited both components, with 91.1% +/- 4.2% of inhibition for the NANC contraction and 62.0% +/- 5.2% of inhibition for the cholinergic contraction (10(-7) M, n = 7). 4. Whereas the inhibitory effects of salbutamol were strongly inhibited by both propranolol (10(-6) M) and ICI 118,551 (10(-6) M), those of BRL 37344 were only slightly, albeit significantly reduced by both propranolol and ICI 118,551, and those of SR 58611A were unaffected by treatment with either beta-adrenoceptor antagonist. An alpha2-adrenoceptor antagonist, yohimbine, did not influence the inhibitory effects of any of the beta-adrenoceptor agonists tested.5. Concentration-response curves to acetylcholine (10-8 to 10-3 M), [Nle10]NKA(4-10) (10-10 to10-6 M) and substance P (10- to 3 x 10-6 M) were also significantly shifted to the right by salbutamol(10-6 M), whereas SR58611A and BRL37344 (10-6 M) had no effect.6. These results suggest that the stimulation of putative beta 3-adrenoceptors exerts a specific prejunctional inhibitory action on NANC excitatory response induced by EFS of the isolated main bronchus of the guinea-pig. They also suggest that a beta2-adrenoceptor agonistic component may be involved in the effects of BRL 37344.

    Topics: Adrenergic beta-Agonists; Albuterol; Animals; Bronchi; Bronchoconstriction; Dose-Response Relationship, Drug; Electric Stimulation; Ethanolamines; Female; Guinea Pigs; In Vitro Techniques; Male; Parasympathetic Nervous System; Receptors, Adrenergic, beta; Receptors, Neurokinin-1; Tetrahydronaphthalenes

1993
Coexistence of beta 1-, beta 2-, and beta 3-adrenoceptors in dog fat cells and their differential activation by catecholamines.
    The American journal of physiology, 1993, Volume: 264, Issue:3 Pt 1

    The existence of a beta 3-adrenoceptor (in addition to classical beta 1- and beta 2-), its involvement in the control of lipolysis and its recruitment by catecholamines were investigated in dog adipose tissue. Isoproterenol, norepinephrine, and the beta 2-selective agonist procaterol fully activated lipolysis in adipocytes (order of potency: isoproterenol > norepinephrine = procaterol). beta 3-Adrenergic agonists stimulated lipolysis with the order of potency: BRL 37344 > CGP 12177 > SR 58611A. Propranolol and bupranolol (nonselective beta-antagonists) antagonized, with a low potency, the effect of BRL 37344, whereas the beta 1-antagonist CGP 20712A and the beta 2-antagonist ICI 118551 were without action. CGP 20712A inhibited the effect of lower concentrations of agonists (0.05 microM isoproterenol, 0.1 microM norepinephrine and 0.1 microM procaterol) with an inhibitory constant (mean Ki) of 0.0075, 0.032 and > 10 microM, respectively. Mean Ki values for the beta 2-antagonist ICI 118551 were 1.744, 1.243, and 0.019 microM. This result indicates that low concentrations of isoproterenol and norepinephrine stimulate lipolysis mainly via beta 1-adrenoceptors in dog fat cells. Inversely, the lipolytic effect of higher concentrations of agonists i.e., 1 microM isoproterenol and catecholamines, was weakly antagonized by CGP 20712A or ICI 118551 while the nonselective beta-antagonists bupranolol and propranolol suppressed the effects with the order of potency expected for a beta 3-adrenoceptor: bupranolol > propranolol. These data indicate 1) the presence of a functional beta 3-adrenoceptor that coexists with beta 1- and beta 2-adrenoceptors in dog fat cells; 2) a separation of the differential potencies of physiological amines in the activation of lipolysis through beta 1-, beta 2-, and beta 3-adrenoceptors; the lipolytic response initiated at low concentrations (submicromolar range) of norepinephrine is primarily mediated by the beta 1-adrenoceptor subtype; and 3) an activation of the beta 3-adrenoceptor that occurs at higher concentrations of catecholamines.

    Topics: Adenylyl Cyclases; Adipose Tissue; Adrenergic beta-Agonists; Adrenergic beta-Antagonists; Animals; Bupranolol; Catecholamines; Cell Membrane; Dogs; Dose-Response Relationship, Drug; Epinephrine; Ethanolamines; Isoproterenol; Norepinephrine; Procaterol; Propanolamines; Propranolol; Receptors, Adrenergic, beta; Tetrahydronaphthalenes

1993
Beta-adrenoceptor agonist stimulation of acid secretion by rat stomach in vitro is mediated by 'atypical' beta-adrenoceptors.
    British journal of pharmacology, 1992, Volume: 106, Issue:3

    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.

    Topics: Adrenergic beta-Agonists; Adrenergic beta-Antagonists; Alprenolol; Animals; Ethanolamines; Gastric Acid; Imidazoles; In Vitro Techniques; Isoproterenol; Male; Propranolol; Rats; Rats, Inbred Strains; Receptors, Adrenergic, beta; Stomach; Tetrahydronaphthalenes

1992