Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Butoxamine”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources
PubMed1987

Drug-induced penile erections in rats: indications of serotonin1B receptor mediation.

The induction of penile erections by a variety of compounds with a direct or indirect effect on serotonin (5HT) receptors was investigated in rats. L-5-Hydroxy-tryptophan (L-5HTP) induced penile erections when co-administered with nialamide and the peripheral decarboxylase inhibitor benserazide, indicating that the site of action for inducing penile erections is within the central nervous system. Penile erections were also induced by the 5HT uptake inhibitors zimelidine, fluoxetine, citalopram, Org 6997, by the 5HT-releasing agent fenfluramine and by the putative 5-HT1B receptor agonist 1-(3'-chlorophenyl)-piperazine (mCPP). The 5HT1A-agonist 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT) did not induce penile erections. The less selective 5HT receptor agonists 5-methoxy-N,N-dimethyl-tryptamine (5MeODMT), 5-methoxytryptamine (5MeOT), dl-lysergic acid diethylamide (LSD) and Ru 24969 were also ineffective. Induction of penile erections by quipazine appeared only when this compound was co-administered with the 5HT2 receptor antagonist pirenperone. Receptor antagonists were tested against penile erections induced by Org 6997. The beta-adrenoceptor antagonists that also have 5HT1 antagonistic properties, (S)-pindolol and dl-propranolol, antagonized Org 6997-induced penile erections but butoxamine and metoprolol did not. Spiperone and pirenperone in doses selective for 5HT1A and 5HT2 receptors respectively were also inactive. Haloperidol, 0.46 mg/kg, partially attenuated penile erections induction. The data are discussed in the light of the hypothesis that penile erections induction by serotonin-mimetic compounds is mediated by 5HT1B receptors in the striatum.

5-Hydroxytryptophan↗
PubMed1984

Cerebrovascular smooth muscle culture. II. Characterization of adrenergic receptors linked to adenylate cyclase.

Cultured and propagated smooth muscle cells contain adenylate cyclase (AC) responsive to catecholamines and their analogues. Isoproterenol and zinterol were the most effective stimulants of AC activity with EC50 = 8.5 X 10(-8)M. They were followed by epinephrine, phenylephrine and norepinephrine (EC50 = 7.5 X 10(-7)M, 6.5 X 10(-6)M and 4 X 10(-6)M, respectively). When the selective antagonists for beta 1 and beta 2 receptors (beta 1-type practolol and atenolol, beta 1/beta 2-type propranolol and beta 2-type butoxamine) were tested against isoproterenol, epinephrine and norepinephrine stimulation of AC activity, the beta 1 in contrast to beta 2 antagonists were found ineffective. The alpha-blockers (phentolamine alpha 1/alpha 2-type antagonists) and yohimbine (alpha 2-type antagonist) alone or in the presence of propranolol did not significantly inhibit the catecholamine-induced enhancement of cAMP formation. On the other hand, prazosine (alpha 1-type antagonist) blocked the stimulatory effect of epinephrine and norepinephrine on AC system. Similarly, the alpha 2-agonist, clonidine, did not affect the catecholamines' stimulated AC activity while alpha 1 agonist, phenylephrine, induced an additive enhancement of norepinephrine production of cAMP. The findings of beta-2- and alpha-1-type adrenergic receptors in the cultured cerebrovascular smooth muscle provide additional support for the implicated involvement of adrenergic innervation in the regulation of cerebral blood flow and/or systemic blood pressure.

Adenylyl Cyclases↗
PubMed1995

Novel evidence that beta adrenoceptors of the medial septal area regulate blood pressure and electrolyte balance.

We investigated the participation of the beta-adrenoceptors of the septa area (SA) in sodium and potassium excretion and urine flow. The alterations in arterial pressure and some renal functions were also investigated. The injection of 2.10(-9) to 16.10(-9) M of isoproterenol, through a cannula permanently implanted into the SA produced a significant dose-dependent decrease in urinary Na+ and K+ excretion and urinary flow. Pretreatment with 16.10(-9) M butoxamine antagonized the effect of 4.10(-9) M isoproterenol but pretreatment with 16.10(-9) M practolol did not abolish the effect of isoproterenol. The beta 2-agonist terbutaline and salbutamol (4.10(-9) M when injected intraseptally also caused a decrease in urine flow and in renal Na+ and K+ excretion. After injection of isoproterenol or salbutamol (4.10(-9) M) into the SA, the arterial pressure, glomerular, filtration rate (GFR) and filtered Na+ were reduced while Na+ fractional reabsorption was increased. The results indicate that the beta 2-adrenoceptors of the SA play a role in the decrease of Na+, K+ and urine flow and this effect may be due to a drop in GFR and filtered Na+ and to the rise in tubular Na+ reabsorption.

Animals↗
PubMed1983

Adenylate cyclase sensitivity to catecholamines and forskolin in rat pia-arachnoid and cerebral microvessels.

Adenylate cyclase in homogenates of perfused pia-arachnoid from the rat brain displayed a sensitivity for activation by dl'isoproterenol, l'epinephrine, l'norepinephrine (NE) and fenoterol that was greater than shown by partial beta2 adrenergic agonists (metaproterenol and salbutamol), or partial beta1 adrenergic agonists (tazolol and dobutamine) and an alpha adrenergic agonist (phenylephrine). The addition of the quanosine triphosphate (GTP) analog, Gpp(NH)p(5'-guanylyl imidodiphosphate) to the enzyme preparations resulted in an increased ability of all agents (except tazolol) to activate adenylate cyclase. The agent, forskolin, exerted a very potent activation of the catalytic site of adenylate cyclase in both pia-arachnoid and cerebral microvessels (capillary fraction). The order of potency for adrenergic antagonists to inhibit NE-induced stimulation of the pial enzyme was: propranolol (mixed beta) greater than butoxamine (beta2) greater than phentolamine (alpha1) greater than practolol (beta1). Subchronic injections of reserpine to rats resulted in a pial enzyme that was hyper-responsive to NE and isoproterenol. Similarly, the capillary enzyme displayed an enhanced activity to NE and dopamine (DA). Both high and low Km forms of cyclic AMP (cAMP) phosphodiesterase were detected in developing and adult pia-arachnoid and capillaries. The addition of a calmodulin fraction plus calcium ions did not elicit activation of the high Km enzyme. Moreover, adenylate cyclase during development was sensitive to activation by NE and forskolin. Thus, the pia-arachnoid possesses an adenylate cyclase receptor-coupled system with a mixed response to catecholamines, but which is primarily beta2 in nature. In addition, this system, as well as the capillaries, possesses a capacity to respond to manipulation of monoamine levels.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1984

Monoamine activation and enkephalin inhibition of adenylate cyclase in dorsal and ventral striatum of the rabbit.

Adrenergic-sensitive adenylate cyclase was found to be present in the nucleus accumbens and ventral caudate of the rabbit, but displayed less activity in the dorsal caudate. In general, stimulation of the enzyme by dopamine (DA) was most sensitive to inhibition by fluphenazine while norepinephrine (NE)-stimulated activity was highly sensitive to both fluphenazine and propranolol. Other selective adrenergic-receptor blocking agents (butoxamine, practolol, yohimbine and prazosine) were more effective in antagonizing the effect of NE as opposed to DA-activation. Activation of adenylate cyclase by NE in the dorsal caudate displayed less sensitivity to these adrenergic antagonists than in the other two areas. Horseradish peroxidase-positive cells were present in the locus coeruleus, following injection into the nucleus accumbens. Activity of basal and guanosine triphosphate (GTP)-sensitive adenylate cyclase was reduced by enkephalins in these three brain regions. This action was reversed by naloxone. Met-enkephalin did not affect either NE- or DA-mediated responses in any area.

Adenylyl Cyclase Inhibitors↗
PubMed1986

The beta 2-adrenoceptor agonists clenbuterol and salbutamol enhance the hypothermic action of 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) in mice by a central mechanism.

The hypothermic response of mice to injection of 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) was enhanced by injection of the beta 2-adrenoceptor agonist clenbuterol with an ED50 of 0.4 mg/kg. This effect of clenbuterol is through a central mechanism since salbutamol, a beta 2-adrenoceptor agonist with poor penetration into the brain, had no effect at a dose of 2 mg/kg, whereas intracerebroventricular injection of clenbuterol (3 micrograms) or salbutamol (2 micrograms), produced a significant enhancement. The enhancing effect of clenbuterol was unaffected by pretreatment with the beta 1-adrenoceptor antagonist metoprolol but was totally antagonised by the beta 2-adrenoceptor antagonist ICI 118,551 and to a lesser extent by butoxamine. Clenbuterol therefore enhances the function of the presynaptic 5-HT1 receptor through a beta 2-adrenoceptor mechanism.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1991

Effects of selective adrenoceptor agonists and antagonists on aggressive behavior elicited by apomorphine, DL-dopa and fusaric acid in REM-sleep-deprived rats.

REM sleep deprivation (REMSD) results in behavioral changes such as the appearance of affective aggression induced by apomorphine (APO) and other dopaminergic agents. REMSD modifies dopamine-mediated behavior as well as the adrenergic receptor sensitivity. This paper evaluates the interaction between these two neurotransmission systems through changes in APO-, DL-DOPA- and fusaric acid (FA)-induced aggressive behavior in REMSD rats pretreated with phentolamine, propranolol, metaraminol, prazosin, clonidine, yohimbine, isoproterenol, butoxamine and maprotiline. Only isoproterenol reduced FA-induced aggressiveness. No specific changes in aggressiveness were noticed with other treatments and not even inhibitors of norepinephrine transmission induced aggressive behavior. It is concluded that norepinephrine had a slight inhibitory action on aggressiveness elicited by dopaminomimetic agents in REMSD rats. Beta-adrenoceptors could be responsible for this effect since only beta-selective drugs reduced aggression. As REMSD reduces beta-adrenoceptor sensitivity, only minor changes in aggressiveness could be observed. It was noted that the three drugs used to induce aggressive behavior elicited different patterns of aggression.

Aggression↗
PubMed1996

Social confrontation and tumor metastasis in rats: defeat and beta-adrenergic mechanisms.

The effect of social confrontation on the susceptibility to metastatic development was studied in rats. An intruder male Fischer 344 (F344) was introduced to a male-female Long-Evans pair and the behavior was recorded during the first 30 min of a 7-h confrontation session. Mammary tumor cells (MADB106), syngeneic to the inbred F344 rat, were injected i.v. to the intruder 1 h after the beginning of the confrontation session, and the lung retention of tumor cells was determined 24 h later. In this tumor model, metastases develop only in the lungs. Retention of tumor cells and the consequent development of lung colonies are known to be highly controlled by the activity levels of natural killer cells during the first 24 h after tumor inoculation but not later. Twenty of the 21 intruders were attacked by resident males and 19 displayed submissive behavior. A significant increase in lung tumor retention was evident in intruders compared to both control groups: home cage and new environment. The magnitude of this increase was higher in intruders that frequently displayed submissive behavior (indicating social defeat). Pretreatment with the beta-adrenergic antagonist, butoxamine, reduced the effects of social confrontation by approximately 50%, and adrenal demedullation almost abolished it without significantly affecting the social interaction. These findings suggest that the nature of intruder-resident interaction, rather than being subdominant or exposure to an unfamiliar environment, has a marked influence on the intruder's susceptibility to metastatic development. These effects of social confrontation seem to be mediated by adrenergic mechanisms, possibly via adrenergic influence on NK function and distribution.

Aggression↗
PubMed1993

Effects of beta-adrenergic blockers on drug-induced tremors.

We studied the effect of various kinds of beta-adrenergic blockers on oxotremorine-, harmaline- and thyrotropin-releasing hormone (TRH)-induced tremors in mice. To investigate what property of beta-blockers plays the main role in suppressing tremor, we employed five beta-blockers (propranolol, atenolol, butoxamine, pindolol, and arotinolol). All drugs suppressed oxotremorine-induced tremors but none reduced harmaline-induced tremors. Even though TRH-induced tremors were decreased significantly only by propranolol and high doses of arotinolol, all drugs had a tendency to reduce the tremor. We concluded that neuropharmacological mechanisms underlying to harmaline-induced tremors were different from those of TRH- and oxotremorine-induced tremors and that features of beta-blockers (beta 1- or beta 2-selectivity, intrinsic sympathomimetic activity, and membrane stabilizing activity) did not primarily contribute to the suppression of tremors.

Adrenergic beta-Antagonists↗
PubMed1980

The use of guinea pig K+-depolarized tracheal chain preparations in beta-adrenoceptor studies.

Guinea pig tracheal chain preparations were K+-depolarized using Krebs solution in which all the Na+ was replaced by an equivalent amount of K+. This caused a sustained contraction of the preparations. Reproducible concentration-response (relaxation) curves to isoprenaline could be obtained provided that the preparations were repolarized by washing in normal Krebs solution between curves. pA2 values for propranolol (8.30) and butoxamine (5.89) were in good agreement with values obtained on other types of tracheal preparation. The maximum relaxation to salbutamol was less than that to isoprenaline and the maxima to both drugs were less than the maximum relaxation of the tissue (to papaverine). It is suggested that K+-depolarized tracheal preparations have no beta-adrenoceptor reserve and may, therefore, be useful in studies designed to compare the efficacies of beta-adrenoceptor agonists.

Animals↗
PubMed1985

Calcium and norepinephrine levels of rat salivary glands after terbutaline, dobutamine or isoproterenol.

Present data show that a dose-related increase in calcium concentration [Ca] of submandibular glands of rat occurred after 6 days of twice daily administration of 25, 50 or 75 mg/kg b. wt. doses of the beta 1-adrenergic agonist, dobutamine, or the beta 2-adrenergic agonist, terbutaline. The beta 1-adrenergic receptor was responsible for mediation of these changes with both agonists since the effects of either agonist were prevented when a 10 mg/kg dose of the beta 1-antagonist, atenolol, was injected 20 min prior to the agonist, and the increase induced by either agonist was not prevented when the beta 1-adrenergic antagonist, butoxamine, was given prior to each agonist. Dobutamine caused more marked increases in [Ca] than did terbutaline. The parotid gland, however, showed a decrease with both agonists, and that caused by dobutamine was greater than that caused by terbutaline. Neither antagonist had any effect on the agonist-induced changes in the parotid gland. Reasons for the differences in response of the two glands are suggested. It does not appear, however, that, as suggested previously, the increase in the [Ca] of the submandibular gland is dependent on depletion of glandular levels of norepinephrine (NE). Of the agonists, only dobutamine caused a decrease in glandular concentration of NE, as well as total NE of the gland. With isoproterenol (ISO), NE concentration of parotid and submandibular was reduced, but with terbutaline only that of parotid was reduced. changes in total glandular NE were not found in either gland with either ISO or terbutaline. Thus, the decrease in concentration was a consequence of the increased mass of gland. With cyclocytidine (CC), both NE concentration and total NE were reduced, even though gland size increased. With reserpine (RES), NE concentration as well as total NE were markedly reduced (87-90%), and no change in gland size occurred. It is suggested, on the basis of present data, that prolonged activation of beta 1-adrenoceptors is the cause of the calcium accumulation, and that reduction in NE is not the cause of the calcium increase, but may only be a coincident event. Even with sympathectomy (here induced by reserpine), activation of beta-receptors over a long period of time is suggested as the cause of the calcium change, not the depletion of NE. The present data also provide the first evidence that CC causes NE depletion.

Adrenergic beta-Agonists↗
PubMed1984

Stimulation of beta 2-adrenergic receptors suppresses sterol synthesis in human mononuclear leukocytes.

The beta-adrenergic receptor mediating the inhibition of sterol synthesis by catecholamines in freshly isolated human mononuclear leukocytes was defined pharmacologically by using selective beta 1- and beta 2-agonists and -antagonists. Incubation of cells for 6 h in a medium containing lipid-depleted serum resulted in a 3-fold increase in the incorporation of [14C]acetate or tritiated water into sterols. The beta-agonist (-)-isoproterenol was approximately equipotent with (-)-epinephrine and (-)-norepinephrine in suppressing sterol synthesis, yielding a sigmoidal log-dose-effect curve. Accordingly, the effects of the catecholamines were reversed by the beta-antagonist (+/-)-propranolol. The beta 2-agonists terbutaline and salbutamol inhibited sterol synthesis by 42 and 26%, respectively, at a concentration of 0.1 mmol/l. Contrary to that, the beta 1-agonists prenalterol and dobutamine had no effect. In accordance with the influence of the agonists, the beta 2-antagonist butoxamine, but not the beta 1-antagonists atenolol, metoprolol and practolol, reversed the catecholamine action on sterol synthesis. The results provide evidence that catecholamines may regulate sterol synthesis by stimulating beta 2-adrenergic receptors.

Adrenergic beta-Agonists↗
PubMed1987

Beta 2-adrenergic regulation of prostaglandin D2 receptor in rabbit platelets.

[3H]Prostaglandin D2 binding to rabbit platelets was increased by about 150% in the presence of beta-adrenoceptor agonist, isoproterenol. The isoproterenol-induced potentiation of the [3H]prostaglandin D2 binding gave a bell-shaped dose-response relationship (maximum response at 3 X 10(-8) M) in a stereospecific manner. Similar and moderate potentiation was obtained with terbutaline. On the other hand, beta-adrenoceptor antagonists such as alprenolol, propranolol and butoxamine (beta 2-specific) had no potentiating effect on [3H]prostaglandin D2 binding; rather, they abolished the isoproterenol-induced increase of [3H]prostaglandin D2 binding. The beta 1-specific antagonist, metoprolol, did not have any effect. Rabbit platelets were found to possess one [3H]prostaglandin D2 binding site (Kd = 6 X 10(-7) M, Bmax = 787 fmol/mg protein). In the presence of isoproterenol at 3 X 10(-8) M, Bmax was increased with unaltering Kd value. Isoproterenol did not increase [3H]prostaglandin E1, [3H]prostaglandin E2 and [3H]prostaglandin F2 alpha bindings to platelets. The potential effect of isoproterenol was mimicked by forskolin, theophylline, dibutyryl cyclic AMP, prostaglandin E1 and prostaglandin I2, but it was abolished by 2', 5'-dideoxyadenosine, an inhibitor of adenylate cyclase, indicating that elevated level of cyclic AMP may be available for the induction of the increase of [3H]prostaglandin D2 binding. Prostaglandin D2-induced cyclic AMP synthesis and antiaggregation activity were also augmented in the presence of isoproterenol. These results suggest a beta 2-adrenoceptor-mediated cyclic AMP-dependent mechanism for the regulation of prostaglandin D2 receptor binding in rabbit platelets.

Adenylyl Cyclase Inhibitors↗
PubMed1995

ATP release evoked by isoprenaline from adrenergic nerves of guinea pig atrium.

Mode and site of release of ATP evoked by isoprenaline were evaluated in the electrically driven left atrial segment of guinea pig. The peak release of ATP 5 min after 1 microM isoprenaline was inhibited by 1 microM propranolol and 1 microM butoxamine, but not by 1 microM atenolol, showing that the ATP release is due to stimulation of the presynaptic beta 2-adrenoceptor by isoprenaline. The maximum ATP release was markedly reduced by Ca2+/calmodulin antagonists, W-7 and trifluoperazine, and by a mitotic inhibitor, vinblastine. Further, the release was similarly inhibited by myosin light chain kinase inhibitors, ML-7 and wortmannin. Nifedipine, a Ca(2+)-channel blocker, decreased the release of ATP evoked by isoprenaline. By contrast, Bay K 8644, a Ca(2+)-channel opener, tended to enhance the ATP release. These findings suggest that isoprenaline produces ATP release from adrenergic nerve terminals of atrium, implying that ATP serves as a co-transmitter.

Adenosine Triphosphate↗
PubMed1994

Inhibitory effect of sodium nitroprusside on the relaxing action of isoproterenol in isolated rat urinary bladder.

1. Isoproterenol caused relaxation of rat detrusor muscles contracted by electrical stimulations. Sodium nitroprusside (SNP) and methylene blue inhibited the relaxation induced by isoproterenol without affecting forskolin-induced relaxation. 2. In the presence of theophylline, zaprinast still potentiated isoproterenol-relaxation. In the presence of butoxamine, a selective beta 2-adrenoceptor inhibitor, but not metoprolol, a selective beta 1-adrenoceptor inhibitor, SNP still inhibited isoproterenol-relaxation. 3. SNP inhibited the relaxation to dobutamine, a beta 1-adrenoceptor agonist but not that to terbutaline, a beta 2-adrenoceptor agonist. The relaxation to dobutamine was also inhibited by methylene blue. Further, in the presence of theophylline, zaprinast still potentiated dobutamine-relaxation. 4. Isoproterenol increased tissue level of cGMP, which was inhibited by propranolol. 5. These results suggest a possibility that, in rat detrusor muscles, isoproterenol causes relaxation due to increases in the level of both cAMP and cGMP.

Animals↗
PubMed1984

Specificity of beta-adrenergic control of lipolysis in swine adipose tissue.

Fenoterol (beta 2-agonist) and several analogs stimulated swine adipose tissue lipolysis in addition to epinephrine, norepinephrine and isoproterenol. Lipolytic activity was inhibited by propranolol (beta 1 + beta 2) greater than metoprolol (beta 1) greater than ICI 118,551 (beta 2) greater than practolol (beta 1) much greater than butoxamine (beta 2) regardless of the agonist used in the test system. The swine adipose adrenoceptor is not readily classified into a beta 1 or beta 2 subtype. It may be unique or the classification systems devised in laboratory animals may not be applicable across species.

Adipose Tissue↗
PubMed2005

The cellular mechanisms involved in the vasodilator effect of nebivolol on the renal artery.

Nebivolol is known as a highly selective beta1-adrenoceptor antagonist. Based on the reported vasodilator effect of nebivolol, we examined the cellular mechanisms by which the drug induces renal artery vasodilation, an issue of potential relevance for condition associated with high blood pressure. To this purpose, myograph and patch-clamp techniques were used. Small mouse renal arteries were placed in the myograph chamber, and after the optimal concentration for the vasodilator effect of nebivolol was established (50 microM), the arteries were further investigated to assess the potential contribution of nitric oxide (NO) and of Ca2+ ions to the nebivolol-induced effect, by exposing the arteries to the specific inhibitors such as N(G)-nitro-L-arginine methylester (L-NAME, 100 microM), ethylenglycol-bis-(beta-amino-ethylen ester) N,N'-tetraacetic acid (EGTA, 4 microM) and thapsigargin (1 microM). The expression of NO synthase was evaluated by the Western-blot technique. Using myograph and patch-clamp techniques applied on intact renal artery, we investigated the role of beta2-adrenoceptors, of myoendothelial junctions and of Ca(2+)-activated K+ channels in the vasodilatory effects of nebivolol, using 100 microM butoxamine, 40 microM 18 beta-glycyrrhetinic acid, 1 mM tetraethylammonium, and 100 nM iberiotoxin, respectively. The results showed that the cellular mechanisms of the vasodilator effect of nebivolol on the renal artery entail (i) activation of the endothelial beta2-adrenoceptor, (ii) participation of [Ca2+]i, (iii) increase in NO and eNOS, and (iv) activation of Ca(2+)-activated K+ channels. The cellular mechanisms underlying vasodilator effect of nebivolol on the artery explain the favorable effect of this drug in hypertension.

Acetylcholine↗
PubMed2005

Beta2-adrenergic receptor stimulation inhibits LPS-induced IL-18 and IL-12 production in monocytes.

We examined the effects of beta2-adrenergic receptor (beta2-AR) agonists on monocyte-derived cytokines, interleukin (IL)-18 and IL-12 production in lipopolysaccharide (LPS)-stimulated monocytes derived from human peripheral blood mononuclear cells (PBMCs), as in vitro model of sepsis. The study found that beta2-AR agonists inhibited IL-18 and IL-12 production in monocytes, and that AR agonist activity was antagonized by the selective beta2-AR antagonist, butoxamine. The selective beta2-AR agonists salbutamol and terbutaline induced a similar inhibitory pattern of IL-18 and IL-12 production. IL-12 production induced by LPS was inhibited by anti-IL-18 Ab, but IL-18 production by LPS was not inhibited by anti-IL-12 Ab, showing that LPS induced IL-18 production without IL-12 production. Therefore, the stimulation of beta2-AR might be beneficial in the treatment of sepsis through inhibiting LPS-elicited IL-18.

Adrenergic beta-2 Receptor Agonists↗