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PubMed2001

beta(2)-adrenergic receptor overexpression increases alveolar fluid clearance and responsiveness to endogenous catecholamines in rats.

beta-Adrenergic agonists accelerate the clearance of alveolar fluid by increasing the expression and activity of epithelial solute transport proteins such as amiloride-sensitive epithelial Na(+) channels (ENaC) and Na,K-ATPases. Here we report that adenoviral-mediated overexpression of a human beta(2)-adrenergic receptor (beta(2)AR) cDNA increases beta(2)AR mRNA, membrane-bound receptor protein expression, and receptor function (procaterol-induced cAMP production) in human lung epithelial cells (A549). Receptor overexpression was associated with increased catecholamine (procaterol)-responsive active Na(+) transport and increased abundance of Na,K-ATPases in the basolateral cell membrane. beta(2)AR gene transfer to the alveolar epithelium of normal rats improved membrane-bound beta(2)AR expression and function and increased levels of ENaC (alpha subunit) abundance and Na,K-ATPases activity in apical and basolateral cell membrane fractions isolated from the peripheral lung, respectively. Alveolar fluid clearance (AFC), an index of active Na(+) transport, in beta(2)AR overexpressing rats was up to 100% greater than sham-infected controls and rats infected with an adenovirus that expresses no cDNA. The addition of the beta(2)AR-specific agonist procaterol to beta(2)AR overexpressing lungs did not increase AFC further. AFC in beta(2)AR overexpressing lungs from adrenalectomized or propranolol-treated rats revealed clearance rates that were the same or less than normal, untreated, sham-infected controls. These experiments indicate that alveolar beta(2)AR overexpression improves beta(2)AR function and maximally upregulates beta-agonist-responsive active Na(+) transport by improving responsiveness to endogenous catecholamines. These studies suggest that upregulation of beta(2)AR function may someday prove useful for the treatment of pulmonary edema.

Adenoviridae↗
PubMed1991

[Pharmacological action of SN-408, a novel long-acting selective beta 2-adrenoceptor agonist].

The bronchodilating effect and other related pharmacological properties of SN-408 were studied in comparison with those of isoproterenol, salbutamol and procaterol. SN-408 caused concentration-dependent relaxation of isolated guinea pig trachea via the beta 2-adrenoceptor. The order of relaxation potency was: procaterol greater than SN-408 greater than or equal to isoproterenol greater than salbutamol, but the duration of the action of SN-408 was far longer than those of other beta-agonists. Positive chronotropic and inotropic actions of SN-408 in isolated guinea pig right atria and left atria were less potent than those of other beta-agonists. In isolated guinea pig lung tissues, SN-408 increased cyclic AMP contents. Also in vivo, SN-408 showed dose-dependent bronchodilating action by i.v. administration in anesthetized guinea pigs and by inhalation in conscious guinea pigs. Bronchodilating actions of SN-408 were less potent than those of procaterol and isoproterenol, but the duration of action of SN-408 was far longer than those of other beta-agonists. SN-408 showed no evidence of the development of tolerance to the bronchodilating action. SN-408 caused small tachycardia in guinea pigs by i.v. and inhalation. SN-408 given i.v. suppressed vascular permeability in mice. These results indicate that SN-408 is a long-acting and selective beta 2-stimulant bronchodilator.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Clinical trial of corticosteroid and beta-2 bronchodilator in acute wheezing infants.

To evaluate the effect of a combination of corticosteroid and beta-2 bronchodilator on acute, young, wheezing patients, a total of 80 patients, ages below 36 months who were hospitalized for this condition during the period November 1988 to March 1990 were studied. They were divided into three groups. Group A consisted of 29 cases, under 12 months old, and treated with hydrocortisone and procaterol; Group B included 23 cases, between 12 and 36 months old, treated as in Group A; Group C, of 28 cases younger than 12 months, received neither drug. The clinical severity scores for Group B were significantly more improved than Group A on days 4 and 5 (p less than 0.05 and p less than 0.05, respectively), and better than that of Group C on days 3, 4, and 5 (p less than 0.05, 0.005, and 0.05, respectively). No significant difference was found between Group A and C from days 1 to 5. The previous wheezy coughing episodes were significantly more frequent in Group B than in Groups A and C (p less than 0.05). Two-thirds of the quick responders to hydrocortisone and procaterol were 12 months old or older. The personal and family allergic history, serum IgE level, and total eosinophil count could not be used as parameter to predict responsiveness to the combined therapy of hydrocortisone and procaterol.

Acute Disease↗
PubMed1986

The modulation of head-twitch behaviour by drugs acting on beta-adrenoceptors: evidence for the involvement of both beta 1- and beta 2-adrenoceptors.

Drugs selective for either the beta 1- or beta 2-adrenoceptor have been investigated for their effects on the head-twitch behaviour induced by L-5-hydroxytryptophan (L-5-HTP) in mice. All four agonists, dobutamine and prenalterol (beta 1-), and salbutamol and procaterol (beta 2-), potentiated the effect of L-5-HTP although they were ineffective in inducing the head-twitch when administered alone. The corresponding antagonists, practolol and metoprolol (beta 1-) and butoxamine and ICI 118,551 (beta 2-), were without effect on the L-5-HTP head-twitch. The antagonists each significantly reduced the effect of the corresponding agonists but, while butoxamine and ICI 118,551 were inactive against dobutamine and prenalterol potentiation, both practolol and metoprolol reduced the effect of salbutamol and procaterol. Thus it is argued that dobutamine and prenalterol potentiation is due to an action at beta 1-adrenoceptors, while at least a component of the potentiating effect of salbutamol and procaterol is exerted through beta 2-adrenoceptors. The lack of effect of the antagonists alone is discussed.

5-Hydroxytryptophan↗
PubMed1982

Characteristics of the lipolytic beta-adrenergic receptors in hamster adipocytes.

Hamster adipocyte beta-adrenergic receptors were characterized by the effect on the lipolysis rate of several selective beta-adrenergic agonists and antagonists. Prenalterol and procaterol, selective beta 1- and beta 2-agonists, respectively, both stimulated the lipolysis rate half-maximally at 1-2 microM, a concentration approximately 100-fold higher than that needed for half-maximal stimulation by isoprenaline. The maximal procaterol effect was similar to that of isoprenaline, while the effect of prenalterol was 40% lower. Submaximally isoprenaline-stimulated lipolysis was half-maximally inhibited by propranolol at 0.2 microM and by atenolol and H 35/25, selective beta 1- and beta 2-antagonists, at 23 and 6 microM concentration, respectively. Highly specific beta 1 and beta 2 stimulation was induced by incubation with prenalterol or procaterol, with simultaneous maximal selective beta 2 or beta 1 inhibition, respectively. The maximal beta 2 stimulation was approximately twice the corresponding beta 1 effect under these conditions, the sum of both effects closely approaching that of maximal nonselective beta-adrenergic stimulation with isoprenaline. Similar results were obtained with the selective beta 2-antagonist, ICI 118,551, or the beta 1-antagonists, pamatolol and practolol. The findings are most easily explained by the existence of a heterogeneous beta 1- and beta 2-adrenergic receptor population on hamster adipocytes.

Adipose Tissue↗
PubMed1994

Pharmacological characterization and anatomical localization of prejunctional beta-adrenoceptors in the rat kidney.

1. The subtype and anatomical localization of beta-adrenoceptors mediating facilitation of stimulus-induced overflow of noradrenaline ('prejunctional beta-adrenoceptors') are not conclusively known to date. The present study was undertaken to characterize these receptors by use of pharmacological methods as well as to define their localization (prejunctional or postjunctional) with radio-ligand binding and autoradiography techniques combined with surgical denervation of the sympathetic innervation to the rat kidney. 2. Exposure of the kidney to (-)-isoprenaline, the nonselective beta-adrenoceptor agonist, resulted in a dose-dependent facilitation of stimulus-induced neurotransmitter overflow. This response was inhibited by propranolol, the beta 1- and beta 2-adrenoceptor antagonist, with a pA2 of 9.20 suggesting that the prejunctional beta-adrenoceptors are not of the beta 3-subtype. 3. The rank order of potency and potency ratios of beta-adrenoceptor agonists at renal prejunctional beta-adrenoceptors (EC50 for agonist/EC50 for (-)-isoprenaline) were: (-)-isoprenaline (1) > procaterol (2) > salbutamol (3) > adrenaline (10) > (+)-isoprenaline (25). However, dobutamine, the beta 1-adrenoceptor agonist, failed to enhance stimulus-induced overflow of noradrenaline. These results are indicative of the presence of beta 2-adrenoceptors as prejunctional beta-adrenoceptors. 4. Facilitation elicited by (-)-isoprenaline and procaterol, the selective beta 2-adrenoceptor agonist, was inhibited by ICI 118,551, the selective beta 2-adrenoceptor antagonist, with pKb values of 9.20 and 9.35, respectively at renal prejunctional beta-adrenoceptors. Similarly, the pKb values of metoprolol, the selective beta 1-adrenoceptor antagonist, at renal prejunctional beta-adrenoceptors were determined to be 6.25 and 6.18 against (-)-isoprenaline and procaterol, respectively. These results suggest the presence of a homogeneous population of beta 2-adrenoceptors as prejunctional beta-adrenoceptors. 5. Radio-ligand binding analysis of renal beta-adrenoceptors revealed the prevalence of the beta 1-subtype as compared to the beta 2-subtype (63% vs 37%). However, surgical denervation of the rat kidney, resulting in more than 90% reduction in renal noradrenaline content, selectively reduced the beta 2-adrenoceptor population by 80%, implying the presence of beta 2-adrenoceptors on renal sympathetic nerve terminals. 6. Autoradiographic analysis demonstrated the presence of beta 1-adrenoceptors on cortical structures such as glomeruli and tubules. beta-Adrenoceptors were found to be present on tubules (minor population), collecting tubules in outer medulla and the adventitia and adventitial-medial border of intraparenchymal branches of the renal artery. Surgical denervation of the rat kidney resulted in the disappearance of Beta2-adrenoceptors associated with the intraparenchymal branches, without affecting the Beta-adrenoceptor populations at other sites. These results support the notion that the Beta2-subtype is present on renal sympathetic nerve terminals and demonstrate that these prejunctional Beta2-adrenoceptors are associated with the renal vasculature and not with renal tubules.7. The results of the present investigation demonstrate that renal prejunctional Beta-adrenoceptors are of the Beta2-subtype in nature. These receptors are present on sympathetic nerve terminals which are associated with the renal vasculature.

Animals↗
PubMed1997

Beta 3-adrenergic receptor-mediated lipolysis and oxygen consumption in brown adipocytes from cynomolgus monkeys.

Primary adipocytes were isolated from axillary brown adipose tissue from adult cynomolgus monkeys. That this tissue contained brown adipocytes was verified by morphological examination and by demonstrating the presence of uncoupling protein messenger ribonucleic acid in the isolated adipocytes. The contributions of beta 1-, beta 2-, and beta 3-adrenergic receptors (AR) to lipolysis and oxygen consumption of isolated brown adipocytes were determined after agonist stimulation. Dose responses were determined using isoproterenol (a nonselective beta-AR agonist), denopamine (beta 1-AR agonist), procaterol (beta 2-AR agonist), and CGP12177A (beta 1- and beta 2-AR antagonist, beta 3-AR agonist). Isoproterenol, denopamine, and procaterol stimulated lipolysis with EC50 values of 4,500, and 83 nmol/L, respectively. Intrinsic activities (relative to isoproterenol maxima) were 100%, 74%, and 59%, respectively. The presence of beta 3-ARs coupled to lipolysis was demonstrated by the activity of CGP12177A (EC50 = 1.6 mumol/L; intrinsic activity = 62%). Isoproterenol stimulated oxygen consumption of brown adipocytes by 75-100% above the basal rate, with an EC50 of 1 mumol/L. Denopamine, procaterol, and CGP12177A stimulated oxygen consumption at a concentration of 100 mumol/L. These results demonstrate that all three beta-adrenergic receptor subtypes are coupled to lipolysis and oxygen consumption in brown adipocytes from cynomolgus monkeys.

Abdomen↗
PubMed1994

TA-2005, a novel, long-acting, and selective beta 2-adrenoceptor agonist: characterization of its in vivo bronchodilating action in guinea pigs and cats in comparison with other beta 2-agonists.

Relaxant effects of the beta 2-selective adrenoceptor agonist TA-2005 on bronchoconstriction in the anesthetized guinea pig and cat were evaluated in comparison with other known beta 2-adrenoceptor agonists. The ED50 values of intravenously administered TA-2005, procaterol, formoterol, isoproterenol, salbutamol, and salmeterol to inhibit the histamine-induced bronchoconstriction of the guinea pigs were 0.024, 0.053, 0.056, 0.099, 0.23, and 2.00 micrograms/kg, respectively, and those in serotonin-challenged cats were 0.019, 0.037, 0.039, 0.042, 0.13, and 0.52 micrograms/kg, respectively, in the same increasing order. When guinea pigs were passively sensitized with anti-ovalbumin antiserum, the ED50 values of TA-2005, formoterol, procaterol, and isoproterenol to inhibit the antigen-induced bronchoconstriction were 0.09, 0.30, 0.65, and 7.0 micrograms/kg, i.v., respectively, while those of TA-2005, procaterol, formoterol, and salbutamol in actively sensitized animals were 0.24, 0.25, 1.40, and 23.0 micrograms/kg. When TA-2005 was administered by inhalation to guinea pigs or by the intraduodenal route to cats, it exhibited a long-lasting inhibitory effect comparable or superior to the effects of salmeterol and formoterol. These data indicate that, among the known beta 2-adrenoceptor agonists examined, TA-2005 exerts the most potent bronchodilating effects with a long duration of action in vivo, and its potency ratios to the other reference drugs were greater in antigen- than spasmogen-induced bronchoconstriction models.

Administration, Inhalation↗
PubMed1985

Studies on the affinity and selectivity of denopamine (TA-064), a new cardiotonic agent, for beta-adrenergic receptors.

Denopamine is a new orally active cardiotonic agent. The present experiment was carried out to characterize the binding affinity and selectivity of this drug for beta-adrenergic receptor subtypes. Binding studies were performed using 3H-dihydroalprenolol as the radioligand. Binding affinities of denopamine and some beta-agonists for rat heart membranes (KiH), which contain predominantly the beta 1-subtype, were in the order of isoproterenol (Iso, 14.1 nM) greater than prenalterol (158) greater than norepinephrine (Nor, 227) greater than or equal to epinephrine (Epi, 248) greater than denopamine (545) greater than or equal to dobutamine (645) greater than procaterol (1440) greater than terbutaline (6420). In rat lung membranes (predominantly beta 2-subtype), the order of potency (KiL) was Iso (20.6 nM) greater than procaterol (70.2) greater than Epi (136) greater than prenalterol (412) greater than dobutamine (735) greater than or equal to Nor (744) greater than denopamine (2205) greater than terbutaline (2500). The beta 1/beta 2-selectivity as judged from the KiL/KiH values was in the order of denopamine (4.1) greater than Nor (3.3) greater than prenalterol (2.6) greater than Iso (1.5) greater than dobutamine (1.1) greater than Epi (0.55) greater than terbutaline (0.39) greater than procaterol (0.05). Practolol, a beta 1-antagonist, showed a high beta 1-selectivity (KiL/KiH = 15.3). In the presence of guanine nucleotide (GTP), the denopamine radioligand competition curve showed a rightward shift, and its Hill coefficient increased like other agonists, although the degree of the shift was less than that observed with full agonists such as Iso. These results essentially correspond with the pharmacological and biochemical properties of denopamine and confirm the beta 1-selectivity and the agonist property of this compound.

Animals↗
PubMed2000

Role of the beta(3)-adrenoceptor in urine storage in the rat: comparison between the selective beta(3)-adrenoceptor agonist, CL316, 243, and various smooth muscle relaxants.

The objective of this study was to compare the effects of a beta(3)-adrenoceptor (beta(3)-AR) agonist on bladder function and cardiovascular parameters in rats with those of several drugs that act on smooth muscle. CL316,243 (beta(3)-AR agonist), isoproterenol (nonselective beta-AR agonist), procaterol (beta(2)-AR agonist), verapamil (Ca(2+) antagonist), and papaverine (antispastic drug) each evoked a concentration-dependent relaxation of the detrusor in vitro. They also reduced bladder pressure in anesthetized rats, the beta-AR agonists apparently being more potent than the other drugs. Atropine (muscarinic antagonist) neither relaxed detrusor strips nor reduced bladder pressure. In anesthetized rats, CL316,243 and atropine each had only a slight influence on blood pressure and heart rate, but isoproterenol, procaterol, verapamil, and papaverine significantly affected cardiovascular function at the same dose range as that required to reduce bladder pressure. In cystometry experiments, CL316,243 (10 microg/kg i.v.), verapamil (1 mg/kg i.v.), and papaverine (1 mg/kg i.v.) all significantly prolonged micturition interval and increased bladder capacity, but did not change the residual urine volume after a micturition contraction. Procaterol (100 microg/kg i.v.) prolonged the micturition interval and increased both bladder capacity and residual urine volume (all significantly). Atropine (100 microg/kg i.v.) reduced micturition pressure and increased residual urine volume (both significantly). Because the human detrusor, like the rat detrusor, relaxes on beta(3)-AR stimulation, we conclude that this beta(3)-AR agonist may have potential in pollakiuria (frequent urination) as a therapeutic agent without cardiovascular side effects.

Adrenergic beta-Agonists↗
PubMed1991

Beta-1 and beta-2 adrenoceptors mediate smooth muscle relaxation in bovine isolated mesenteric lymphatics.

The relaxant effects of beta adrenoceptor agonists were investigated in isolated bovine mesenteric lymphatics which had been contracted by 5-hydroxytryptamine. Addition of isoproterenol (a nonselective beta agonist), denopamine (a selective beta-1 agonist) and procaterol (a selective beta-2 agonist) caused concentration-dependent relaxations in the lymphatic preparations. There was no significant difference in the relaxant responses to the beta adrenoceptor agonists between the preparations with and without endothelium. Treatment with 10(-7) to 3 x 10(-6) M metoprolol (a selective beta-1 antagonist) shifted the concentration-response curve for denopamine to the right, whereas 10(-9) to 3 x 10(-8) M ICI 118,551 (a selective beta-2 antagonist) did not affect the relaxant response to denopamine. The relaxations of bovine mesenteric lymphatics induced by isoproterenol were suppressed by both metoprolol and ICI 118,551. The procaterol-induced relaxations were inhibited by 10(-9) to 3 x 10(-8) M ICI 118,551 but not by 10(-7) to 3 x 10(-6) M metoprolol. Schild plot analyses showed that the slope and pA2 values for metoprolol against denopamine were 1.10 and 7.59, respectively, and that those for ICI 118,551 against procaterol were 0.91 and 9.96. These results suggest that both beta-1 and beta-2 adrenoceptors are located on the smooth muscle cells in bovine mesenteric lymphatics and that stimulation of either receptor produces a marked relaxation.

Adrenergic beta-Agonists↗
PubMed1990

Effects of vasoconstrictive and vasodilative agents on lymphatic smooth muscles in isolated canine thoracic ducts.

A study was made of the isometric responses of isolated canine thoracic ducts to several physiological vasoactive substances. Contractions of the lymphatic smooth muscles were induced by epinephrine, norepinephrine, 5-hydroxytryptamine, histamine (HIS) and prostaglandin F2 alpha in a dose-dependent manner. The decreasing order of potency in the contractile responses was as follows: epinephrine greater than norepinephrine greater than 5-hydroxytryptamine much greater than HIS not equal to prostaglandin F2 alpha. There were no significant regional differences in the responses to vasoconstrictive agents. Phenylephrine, xylazine and clonidine caused a dose-dependent contraction in the lymphatic preparations. Prazosin (10(-8) to 10(-7) M) inhibited the phenylephrine-induced vasoconstriction in a competitive manner. Xylazine-induced responses were inhibited competitively by yohimbine (10(-8) to 10(-7) M). These results suggest that both alpha-1 and alpha-2 adrenoceptors are located on the lymphatic smooth muscles of canine thoracic ducts. On the other hand, acetylcholine, isoproterenol, HIS, adenosine and ATP caused dose-dependent relaxations in canine thoracic ducts precontracted by 10(-5) M norepinephrine. The decreasing order of potency in the relaxant responses was as follows: acetylcholine much greater than isoproterenol much greater than adenosine not equal to HIS not equal to ATP. There were no significant regional differences in the relaxant responses to the agents. Procaterol, salbutamol, dobutamine and denopamine caused a dose-dependent relaxation of isolated canine thoracic ducts. Propranolol (10(-9) to 10(-8) M) inhibited procaterol- and dobutamine-induced vasorelaxations in a competitive manner. Metoprolol (10(-8) to 10(-7) M) inhibited only the dobutamine-induced vasorelaxation, but did not significantly influence the procaterol-induced response.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Beta-adrenoceptor desensitization in a model of experimental asthma in guinea-pigs.

We investigated the possible occurrence of the desensitization of pulmonary beta-receptors in a model of experimental asthma such as the ovalbumin sensitized guinea-pig. Although some differences were observed between normal and asthmatic guinea-pigs, the desensitization procedure (isoproterenol (ISO) 10(-6) M x 20 min x 2) markedly impaired the relaxing capacity of ISO, epinephrine (EPI) and procaterol. With the beta 2 agonist procaterol, the sensitized tissues seemed to be more sensitive compared to normal. In parallel, the desensitization procedure produced a greater decrease in the relaxing capacity of procaterol in the sensitized tracheas. On the other hand, the two unselective beta-agonists (ISO and EPI) did not seem to discriminate between the two experimental conditions used. These data suggest that the immunological disturbance due to the active sensitization may induce a modification in beta-adrenoceptor reactivity. The results obtained with EPI after anaphylactic challenge are in agreement with this. In fact, the relaxing capacity of EPI was markedly reduced by antigen challenge.

Adrenergic beta-Agonists↗
PubMed1995

Effects of beta adrenoceptor agonists and antagonists on adrenal catecholamine release in response to splanchnic nerve stimulation in anesthetized dogs: role of beta-1 and beta-2 adrenoceptors.

The present study was performed to examine whether beta adrenoceptor agonists and antagonists modify the release of adrenal catecholamine (CA) in response to splanchnic nerve stimulation (SNS) in anesthetized dogs, in order to elucidate the beta adrenoceptor-mediated modulation of adrenal CA release. SNS at 3 Hz produced marked increases in both epinephrine and norepinephrine output determined from adrenal venous blood. Atenolol (10, 30 and 100 micrograms/kg, i.v.) and CGP20712A (10 and 30 micrograms/kg, i.v.), selective beta-1 adrenoceptor antagonists, significantly enhanced the SNS-induced increases in CA output. Neither ICI118551 (10, 30 and 100 micrograms/kg, i.v.), a selective beta-2 adrenoceptor antagonist, nor nadolol (10, 30 and 100 micrograms/kg, i.v.), a nonselective beta adrenoceptor antagonist, affected the SNS-induced increases in CA output. After the treatment with ICI118551 (100 micrograms/kg, i.v.), atenolol (10, 30 and 100 micrograms/kg, i.v.) failed to enhance the SNS-induced increases in CA output. On the other hand, neither isoproterenol (0.03 and 0.1 micrograms/kg/min, i.v.) nor the selective beta-2 adrenoceptor agonist procaterol (0.03 and 0.1 micrograms/kg/min, i.v.) affected the SNS-induced increases in CA output. After the treatment with atenolol (100 micrograms/kg, i.v.), both isoproterenol (0.03 micrograms/kg/min, i.v.) and procaterol (0.03 micrograms/kg/min, i.v.) enhanced the SNS-induced increases in CA output. The enhancing effects of isoproterenol and procaterol were abolished by ICI118551 (100 micrograms/kg, i.v.). These results indicate that activation of beta-2 adrenoceptors facilitates the SNS-evoked release of CA from the dog adrenal medulla under the condition in which beta-1 adrenoceptors are blocked, and they suggest that activation of beta-1 adrenoceptors inhibits the beta-2 adrenoceptor-mediated facilitation process of adrenal CA release.

Adrenal Glands↗
PubMed2002

Effects of beta(3)-adrenoceptor stimulation on prostaglandin E(2)-induced bladder hyperactivity and on the cardiovascular system in conscious rats.

AIMS: To investigate the effects of selective beta(2)- and selective beta(3)-adrenoceptor (AR) agonists on prostaglandin (PG) E(2)-induced bladder hyperactivity in conscious free-moving rats. METHODS: Female Sprague-Dawley rats were anesthetized for implantation of bladder, intravenous, and intra-arterial catheters. The effects of a beta(3)-AR agonist (CL316,243) on cystometric and cardiovascular parameters were assessed in conscious rats. Intravesical instillation of PGE(2) (20-60 microM, 6 mL/hr) in conscious rats produced a concentration-dependent increase in voiding frequency. RESULTS: In this model i.v. CL316,243 (beta(3)-AR agonist) reduced basal bladder pressure, increased micturition volume, and prolonged micturition interval in a dose-dependent manner, without affecting threshold pressure or micturition pressure. On the other hand, i.v. procaterol (beta(2)-AR agonist) did not counteract the bladder hyperactivity. Atropine (muscarinic antagonist) reduced micturition pressure and micturition volume, and shortened micturition interval. CL316,243 slightly decreased mean blood pressure and increased heart rate only when given at high doses (10 and 100 microg/kg, i.v.). In contrast, procaterol caused a significant decrease in mean blood pressure and a significant increase in heart rate. Atropine significantly increased heart rate. CONCLUSIONS: The present results clearly demonstrated that the beta(3)-AR agonist prolonged the micturition interval without producing significant cardiovascular side effects. The human detrusor, like the rat detrusor, relaxes on beta(3)-AR stimulation. Provided that these results are valid in humans, selective beta(3)-AR agonists might be clinically useful for controlling a certain type of bladder overactivity.

Adrenergic beta-2 Receptor Agonists↗
PubMed1997

Modulation of pacemaker activity in sheep cardiac Purkinje fibers by stimulation of beta-adrenoceptor subtypes.

The electrophysiological effects mediated by beta 1- and beta 2-adrenoceptors in spontaneously active sheep cardiac Purkinje fibers were investigated using the non-selective agonist (-)-isoproterenol (IPN) and the selective agonists (-)-noradrenaline (beta 1) and procaterol (beta 2) in the absence and presence of the selective antagonists bisoprolol (beta 1) and ICI 118,551 (beta 2). IPN (0.01 mumol/l) increased the spontaneous rate by 54% and the slope of diastolic depolarization by 68% of the respective control values. Further, IPN increased the action potential duration at -20 mV (APD -20 mV) from 96 to 154 ms, reduced the APD-70 mV by 17% and the duration of the diastole by 39% and slightly hyperpolarized the maximum diastolic potential. These effects were partially inhibited by ICI 118,551 (0.03 mumol/l), diminished by bisoprolol (0.1 mumol/l) and almost completely blocked by the combination of both antagonists. Concentration response curves of IPN were influenced by the selective antagonists as follows: ICI 118,551 (0.03 mumol/l) shifted the curves to the right by 0.2-0.4 log units and increased the slope factor. Bisoprolol (0.1 mumol/l) induced a greater shift to the right by 1.1-1.5 log units. Combination of bisoprolol with ICI 118,551 shifted the curves to the right by 1.5-1.7 log units. Noradrenaline (0.3 mumol/l) elicited similar actions as IPN. Bisoprolol (0.1 mumol/l) shifted the concentration response curves of noradrenaline to the right by 1.1-1.9 log units. Actions of procaterol (0.1 mumol/l) were weak, attained only 15-35% of the maximal effects of IPN and could be blocked by ICI 118,551 (0.03 mumol/l). These results show that the increase of pacemaker activity induced by catecholamines in sheep cardiac Purkinje fibers is predominantly mediated by stimulation of beta 1-receptors. However, contribution of beta 2-receptor mediated effects could be demonstrated.

Adrenergic alpha-Agonists↗
PubMed1991

Evidence for the existence of postsynaptic beta-1 and beta-2 adrenoceptors in isolated simian facial veins.

With the use of a steel cannula inserting method, the actions of the beta-adrenoceptor agonists, noradrenaline (NA, a mixed agonist), isoprenaline (a mixed agonist), dobutamine (a selective beta-1 agonist), salbutamol, and procaterol (selective beta-2 agonists), were investigated on isolated and perfused simian facial veins. Each beta-agonist usually induced a vasodilation in a dose-related manner in non-preconstricted vessel preparations. The rank order of potency was isoprenaline much greater than NA greater than dobutamine greater than salbutamol greater than procaterol. NA- and isoprenaline-induced vasodilations were inhibited by either metoprolol (a selective beta-1 adrenoceptor antagonist) or ICI 118,551 (a selective beta-2 antagonist). After beta-1 blockade, NA produced a vasoconstriction which was readily blocked by bunazosin (an alpha-1 antagonist). Dobutamine-induced vasodilations were strongly suppressed by metoprolol and slightly blocked by ICI 118,551. Salbutamol-induced vasodilations were blocked by metoprolol, while ICI 118,551 more markedly inhibited these dilations. From these results, it was concluded that there are abundant beta-adrenoceptors and predominantly beta-1 adrenoceptors in isolated simian facial veins.

Adrenergic beta-Agonists↗
PubMed1988

Role of chemical mediators after antigen and exercise challenge in children with asthma.

Changes in chemical mediators after antigen challenge and exercise challenge tests were studied in children with asthma. Chemical mediators studied after antigen challenge and exercise challenge included histamine, leukotrienes (LTB4, LTC4, and LTD4), and neutrophil chemotactic factor of anaphylaxis (NCA). The pharmacologic modification of immediate and late-phase reactions was evaluated for procaterol (beta 2-agonist), cromolyn sodium, and prednisolone. Histamine levels were noted to rise in patients who had a dual response of a mild to moderate nature, but did not change in patients who had severe asthma. During exercise challenge cromolyn sodium inhibited both immediate and late-phase reactions but also inhibited plasma generation of NCA. Prednisolone, on the other hand, did not affect immediate reactions, but blocked late-phase reactions to exercise and also decreased NCA generation. Procaterol inhibited the generation of LTD4 and also inhibited NCA when compared with placebo. Exercise challenge did not alter levels of plasma histamine or of LTB4 or LTC4.

Adolescent↗