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 163 records · Page 9Linked to original sources
PubMed2004

cAMP-independent mechanism is significantly involved in beta2-adrenoceptor-mediated tracheal relaxation.

The role of cAMP in the beta2-adrenoceptor-mediated relaxation in response to salbutamol was examined in guinea pig tracheal smooth muscle. The concentration-dependent salbutamol-induced relaxation was antagonized in a competitive fashion by a beta2-selective adrenoceptor antagonist, butoxamine, with a pA2 value of 6.90. Salbutamol (10 microM) elevated the tracheal smooth muscle cAMP content by about fivefold, a response which was significantly inhibited by an adenylyl cyclase inhibitor, 9-(tetrahydro-2-furanyl)-9H-purin-6-amine (SQ 22,536, 100 microM). However, the salbutamol-elicited relaxation was not diminished by SQ 22,536 (100 microM). These results provide evidence for the first time that a cAMP-independent mechanism(s) is involved in beta2-adrenoceptor-mediated tracheal smooth muscle relaxation in the guinea pig.

Adrenergic beta-2 Receptor Agonists↗
PubMed2003

Interaction between noradrenaline or adrenaline and the beta 1-adrenergic receptor in the nervous system triggers early metamorphosis of larvae in the ascidian, Ciona savignyi.

Molecular mechanisms underlying the metamorphosis of larvae, e.g., ligand and receptor interaction, have to be determined and roles for the nervous system in marine invertebrates are not well understood. We report here that treatment of swimming larvae of the ascidian Ciona savignyi with noradrenaline or adrenaline promoted morphological changes in early metamorphosis, e.g., tail resorption. Antagonists of the beta-adrenergic receptor, propranolol, and the beta(1)-adrenergic receptor, metoprolol, inhibited the noradrenaline-induced tail resorption, while an antagonist of the alpha-adrenergic receptor, phentolamine, and of the beta(2)- adrenergic receptor, butoxamine, had no inhibitory effects. In addition, a selective agonist of the beta-adrenergic receptor, isoproterenol, the concentration of which was lower than the effective concentration of the neurotransmitters, facilitated tail resorption. Immunohistochemical studies, using an anti-dopamine-hydroxylase antibody, showed that neurotransmitters such as noradrenaline and adrenaline localized around the brain vesicle of the larvae during metamorphosis. The beta(1)-adrenergic receptor stained with antibodies was localized on the nervous system. Temporal expression of the beta(1)-adrenergic receptor was intense in the nervous system in the larvae competent for metamorphosis. We propose that interactions between noradrenaline or adrenaline and the beta(1)-adrenergic receptor in the nervous system mediate the process of metamorphosis of Ciona larvae.

Adrenergic alpha-Antagonists↗
PubMed1999

The role of beta 2-adrenergic vascular receptors in the peripheral vasodilation caused by 17 beta-estradiol in anesthetized pigs.

It has been previously shown in anesthetized pigs that intravenous infusion of 2 microg/h of 17beta-estradiol primarily dilated renal, iliac and coronary circulations, while higher doses of the hormone were required to cause vasodilation also in the mesenteric vascular bed. In the same experimental model, a tonic beta2-adrenoceptor mediated vasodilation, which could be argued to attenuate the vasodilator effect of 17beta-estradiol, has been described. The present study was planned to investigate the role of beta2-adrenergic receptors in the hemodynamic responses of renal and mesenteric vascular beds to 17beta-estradiol. Changes in flow caused by intravenous infusion of 2 microg/h of the hormone at constant heart rate and aortic blood pressure in the left renal and superior mesenteric arteries were assessed using electromagnetic flowmeters. In six pigs, infusion of 17beta-estradiol caused an increase in renal blood flow, which averaged 12.1% of the control values, without affecting mesenteric blood flow. In the same pigs, after hemodynamic variables had returned to the baseline values, blockade of beta2-adrenergic receptors with butoxamine caused an increase in aortic blood pressure and an increase in renal and mesenteric resistance. The subsequent infusion of 17beta-estradiol elicited increases in renal and mesenteric blood flow which respectively averaged 19.6% and 12.8%. Therefore, the present study in anesthetized pigs have shown that the vasodilator responses of the renal and mesenteric circulations to 17beta-estradiol were attenuated and even masked by a tonic beta2-adrenoceptor mediated vasodilation. This indicates that some vasodilator effects elicited by normally used replacement doses of the hormone may not be apparent.

Adrenergic beta-Antagonists↗
PubMed1996

Peripheral beta-adrenoreceptors and stress-induced hypercholesterolemia in rats.

Three experiments were conducted examining the contribution of beta-adrenergic receptors to stress-induced cholesterol increases. Rats were exposed to 3 90-min sessions of inescapable tailshock, or left undisturbed in their home cage. Propranolol, a nonselective beta-blocker, attenuated the stress-induced cholesterol increase when administered prior to the daily shock session. Atenolol, a beta-1 specific antagonist, also attenuated the stress-induced cholesterol increase. Butoxamine, a beta-2 specific antagonist, had no effect on the stress-induced cholesterol increases. Results are discussed in terms of catecholamine-stimulated free fatty acid (FFA) release as a potential mechanism for producing stress-induced hypercholesterolemia.

Adrenergic beta-Antagonists↗
PubMed1996

Contraction and relaxation responses of femoral artery and aorta to norepinephrine in young rats.

1. In femoral artery of 3-week-old rats, norepinephrine (NE) at 1 nM-0.1 microM concentration-dependently produced a contraction but, at higher concentrations (0.3-30 microM), NE relaxed the tissue. 2. In aorta of the 3-week-old rat, NE elicited a contraction at 1 nM to 0.3 microM and a relaxation at 1 microM and higher. 3. The magnitude of the NE-induced relaxation in the aorta was much less than that in the femoral artery. 4. Atenolol (a beta(1)-selective antagonist) modulated these NE responses in the femoral artery and butoxamine (a beta(2)-selective antagonist) in the aorta. 5. Subcutaneous application of propranolol and isoproterenol for 10 days in 4-week-old rats sensitized and desensitized the NE-induced relaxation, respectively. 6. It is suggested that, in the young rat, beta(1)- and beta(2)-adrenoceptors contribute the NE-induced relaxation in the femoral artery and aorta, respectively, and that beta-adrenoceptors may contribute to the limitation of NE-induced vasoconstriction in certain types of vascular beds.

Adrenergic beta-1 Receptor Antagonists↗
PubMed2004

G-protein-coupled receptor chromatographic stationary phases. 2. Ligand-induced conformational mobility in an immobilized beta2-adrenergic receptor.

Membranes from a HEK-293 cell line expressing the beta(2)-adrenergic receptor (beta(2)-AR) have been immobilized on an artificial membrane liquid chromatographic stationary phase. The resulting phase was packed into a glass column (1.8 x 0.5 (i.d.) cm) and used in on-line chromatographic system. Frontal displacement affinity chromatography was used to determine the dissociation constants (K(d)) of CGP 12177A (552.6 nM) and (S)-propranolol (84.3 nM). Zonal displacement chromatography using CGP 12177A as the marker and racemic mixtures of the antagonists nadolol and propranolol demonstrated that the immobilized beta(2)-AR retained its ability to specifically bind these compounds. Similar experiments with (R)- and (S)-propranolol demonstrated that the immobilized receptor retained its enantioselectivity as (S)-propranolol displaced the CGP 12177 marker to a great extent that the (R)-enantiomer. The addition of the agonist butoxamine to the mobile phase increased the retention of the CGP-12177A as did the addition of the agonist fenoterol. These results indicate that the immobilized beta(2)-AR retained its ability to undergo ligand-induced conformational changes. The data from this study suggest that the immobilized beta(2)-AR can be used to screen for ligand binding interactions in both the resting and active states of the receptor.

Adrenergic beta-Antagonists↗
PubMed1990

Differential control of glycogenolysis and flow by arterial and portal acetylcholine in perfused rat liver.

The effects of acetylcholine on glucose and lactate balance and on perfusion flow were studied in isolated rat livers perfused simultaneously via the hepatic artery (100 mmHg, 25-35% of flow) and the portal vein (10 mmHg, 75-65% of flow) with a Krebs-Henseleit bicarbonate buffer containing 5 mM-glucose, 2 mM-lactate and 0.2 mM-pyruvate. Arterial acetylcholine (10 microM sinusoidal concentration) caused an increase in glucose and lactate output and a slight decrease in arterial and portal flow. These effects were accompanied by an output of noradrenaline and adrenaline into the hepatic vein. Portal acetylcholine elicited only minor increases in glucose and lactate output, a slight decrease in portal flow and a small increase in arterial flow, and no noradrenaline and adrenaline release. The metabolic and haemodynamic effects of arterial acetylcholine and the output of noradrenaline and adrenaline were strongly inhibited by the muscarinic antagonist atropine (10 microM). The acetylcholine-dependent alterations of metabolism and the output of noradrenaline were not influenced by the alpha 1-blocker prazosin (5 microM), whereas the output of adrenaline was increased. The acetylcholine-dependent metabolic alterations were not inhibited by the beta 2-antagonist butoxamine (10 microM), although the overflow of noradrenaline was nearly completely blocked and the output of adrenaline was slightly decreased. These results allow the conclusion that arterial, but not portal, acetylcholine caused sympathomimetic metabolic effects, without noradrenaline or adrenaline being involved in signal transduction.

Acetylcholine↗
PubMed1991

Control of glycogenolysis and blood flow by arterial and portal adrenaline in perfused liver.

In isolated liver from fed rats, simultaneously single-pass-perfused via both the hepatic artery (80 mmHg, 30-35% flow) and the portal vein (10 mmHg, 70-65% flow), adrenaline was infused either singly or jointly via the hepatic artery or the portal vein in the absence or presence of the alpha 1-blocker prazosin and the beta 2-blocker butoxamine. It was found that: (1) arterial adrenaline caused increases in glucose and lactate output which were slower in onset, smaller in peak height but longer in duration than did portal adrenaline; (2) arterial adrenaline elicited a much more pronounced decrease in flow and increase in pressure in the ipsilateral vessel than did portal adrenaline, and arterial, but not portal, adrenaline elicited qualitatively similar alterations also in the contralateral vessel; (3) arterial adrenaline caused metabolic changes mainly via alpha 1-receptors, with beta 2-receptors playing a permissive role via haemodynamic alterations, whereas portal adrenaline acted only via alpha 1-receptors; (4) arterial adrenaline decreased arterial flow via alpha 1-receptors counteracted via beta 2-receptors and operated on portal flow as portal adrenaline only via alpha 1-receptors; and (5) arterial adrenaline was extracted to a far greater extent than portal adrenaline. The results indicate that the hepatic artery and the portal vein can function as independent sites of hormonal signal input, which interact by complex, still undefined, mechanisms.

Animals↗
PubMed1995

Evidence for receptor and G-protein regulation of a phosphatidylethanolamine-hydrolysing phospholipase A1 in guinea-pig heart microsomes: stimulation of phospholipase A1 activity by DL-isoprenaline and guanine nucleotides.

While evidence has been presented for the receptor-mediated activation of phospholipases A2, C and D, the activation of phospholipase A1 subsequent to receptor activation has not been established. Phospholipase A1-catalysed hydrolysis of 1-palmitoyl-2-linoleoyl-glycerophosphoethanolamine (GPE) by guinea-pig heart microsomes was stimulated 40-60% by isoprenaline. This isoprenaline-mediated increase in activity was blocked by propranolol and butoxamine, a specific beta 2-adrenergic antagonist, but not by atenolol, a specific beta 1-adrenergic antagonist. Neither clonidine nor phenylephrine, alpha 1- and alpha 2-adrenergic agonists respectively, had a stimulatory effect on the hydrolysis of the PE substrate. Guanosine 5'(-)[gamma-thio]triphosphate (GTP[S]) and guanosine 5'(-)[beta,gamma-imido]triphosphate, but not guanosine 5'(-)[beta-thio]diphosphate (GDP[S]) or adenosine 5'(-)[gamma-thio]triphosphate, stimulated the hydrolysis of 1-palmitoyl-2-linoleoyl-GPE by phospholipase A1. GDP[S] inhibited the isoprenaline-mediated stimulation of phospholipase A1 activity. Phospholipase A1 hydrolysis of 1-palmitoyl-2-linoleoyl-GPE was not dependent on cations; however, the stimulatory effects of isoprenaline and GTP[S] on the hydrolytic activity were abolished by cation chelators. The above data suggest that phospholipase A1 activity in guinea-pig heart microsomes is activated by the binding of isoprenaline to beta 2-adrenergic receptors. Furthermore the stimulation of phospholipase A1 activity by the agonist may be mediated via activation of G-proteins.

Adrenergic beta-Agonists↗
PubMed1994

Adrenergic receptors on cultured rat epididymal cells: regulation of Cl- conductances.

Adrenergic regulation of epididymal Cl- currents was studied by the whole-cell patch-clamp technique using various alpha- and beta-receptor agonists and antagonists in primary cultured rat cauda epididymal cells. Cl- currents could be activated with varying frequency by noradrenaline (primarily alpha- and beta 1-adrenoceptor-selective agonist, 1-5 microM), isoprenaline (nonselective beta-adrenoceptor agonist, 5 microM), salbutamol (beta 2-adrenoceptor-selective agonist, 2 microM), and phenylephrine (alpha 1-adrenoceptor-selective agonist, 1-2 microM). Noradrenaline alone elicited Cl- current activation in 85% of the cells examined. In the presence of phentolamine (nonselective alpha-adrenoceptor antagonist, 15 microM), noradrenaline elicited Cl- current activation in 63% of the cells examined, whereas noradrenaline-induced activation was observed in 33% of the cells examined in the presence of both atenolol and butoxamine (beta 1- and beta 2-adrenoceptor antagonists, respectively, 10 microM). In 27% of single cells examined, a second current activation in response to salbutamol was observed after the first response to phenylephrine. When the order of stimuli was reversed, dual activation was also observed in 22% of the single cells examined, indicating the presence of both alpha- and beta-adrenoceptors in single epididymal cells. Profiles of time- and voltage-dependent Cl- current upon activation by different adrenoceptor agonists exhibited characteristics similar to those previously reported for Ca2+ and cAMP-activated Cl- currents, suggesting that regulation of epididymal Cl- conductances could be mediated by different adrenoceptor subtypes involving Ca2+ and cAMP as intracellular second messengers.

Adrenergic alpha-Agonists↗
PubMed2006

A genetic analysis of opioid-induced hyperalgesia in mice.

BACKGROUND: Opioid-induced hyperalgesia (OIH) is a syndrome of increased sensitivity to noxious stimuli, seen after both the acute and chronic administration of opioids, that has been observed in humans and rodent models. This syndrome may reduce the clinical utility of opioids in treating acute and chronic pain. METHODS: In these studies, the authors measured the propensity of 15 strains of inbred mice to develop mechanical manifestations of OIH. These data were subjected to in silico genetic analysis, which resulted in the association of haplotypic blocks within or near several known genes. Both pharmacologic agents and transgenic mice were used to confirm the functional association of the most strongly linked gene with OIH. RESULTS: Both baseline mechanical nociceptive thresholds and the percentage changes in these thresholds after 4 days of morphine treatment were found to be highly strain dependent. The haplotypic blocks most strongly associated with the mechanical OIH data were located within the beta2 adrenergic receptor gene (beta2-AR). Using the selective beta2-AR antagonist butoxamine, the authors observed a dose-dependent reversal of OIH. Furthermore, deletion of the beta2-AR gene sharply reduced the mechanical allodynia present after morphine treatment in the wild-type mouse strain. Analysis of the associated beta2-AR haplotypic block identified single nucleotide polymorphisms potentially explaining in part the strain specific differences in OIH. CONCLUSIONS: Genetic variants of the beta2-AR gene seem to explain some part of the differences between various strains of mice to develop OIH. The association of this gene with OIH suggests specific pharmacologic strategies for reducing the impact of OIH on patients consuming opioids.

Adrenergic beta-Antagonists↗
PubMed1984

Adrenergic modulation of erythropoiesis: in vitro studies of colony-forming cells in normal and polycythaemic man.

The effect of hormonal interactions on human erythroid colony growth has been studied using the beta adrenergic agonist, isoproterenol. The growth of colonies derived from both erythroid burst-forming cells (BFU-E) and erythroid colony-forming cells (CFU-E) was enhanced in the presence of isoproterenol. While isoproterenol was effective at all concentrations of erythropoietin (Ep) in cultures of marrow cells, an increase in BFU-E-derived colonies in peripheral blood cultures could be detected only at suboptimal levels of Ep concentrations. The isoproterenol effect was blocked by an agent with beta 2 receptor specificity (butoxamine), and L-isomeric configuration (L-propranolol). The stimulatory effect appeared to be mediated by a receptor different from that for Ep or for phytohaemagglutinin-stimulated leucocyte conditioned medium. Circulating BFU-E from eight patients with polycythaemia vera were also studied. Those colonies which grew in the absence of added Ep increased with isoproterenol; in cultures from normal subjects and in patients with secondary erythrocytosis, agonist stimulation was seen only in the presence of Ep. These studies provide evidence that the growth of both normal and neoplastic erythroid progenitors may be modulated by hormonal interactions.

Butoxamine↗
PubMed1993

Beta 2-adrenoceptor stimulation augments the IL-4-induced CD23 expression and release and the expression of differentiation markers (CD14, CD18) by the human monocytic cell line, U 937.

The effect of beta 2-adrenoceptor agonists and interleukin-4 (IL-4) on the CD23 expression on, and release from, the human promonocytic cell line, U 937, was investigated. As assessed by flow cytometry, incubation of U 937 cells in the presence of salbutamol, fenoterol or IL-4 induced a concentration- and time-dependent increase in CD23 expression, that was maximal after 48 hr and followed by a decrease thereafter. In addition, salbutamol potentiated the effect of IL-4, the optimal concentration of the drug being a function of the concentration of this cytokine. This synergy between IL-4 and beta 2-adrenoceptor agonists was also observed for the release of the soluble form of CD23. The effect on CD23 expression of salbutamol and fenoterol, but not of IL-4, was blocked in the presence of D,L-propranolol (1 microM) or butoxamine (1 microM). The alpha-adrenoceptor agonist, norepinephrine (1 microM), was ineffective in inducing CD23 expression or potentiating the one evoked by IL-4. Salbutamol down-regulated the expression of Fc gamma RI (CD64) and Fc gamma RII (CD32) whereas IL-4 was ineffective. Only when added together at the onset of the culture did salbutamol and IL-4 induce, after 48 hr, the expression of the monocyte marker, CD14. The expression of CD18 was up-regulated in response to salbutamol either alone or in combination with IL-4, this cytokine alone being inefficient. These data suggest that IL-4 and beta 2-adrenoceptor agonists induce differentiation of U 937 cells into monocyte-like cells.

Adrenergic beta-Agonists↗
PubMed1996

Acetylcholine-induced bronchoconstriction modified by noise exposure in normal but not in sensitized guinea-pigs.

1. The acute (6h) exposure of guinea-pigs to white noise (110 dB) as a stress stimulus, reduced bronchial reactivity to acetylcholine (Ach) (3-1000 micrograms kg-1 i.v.) in anaesthetized animals. 2. The hyporesponsiveness to Ach in stressed animals was not confirmed in vitro on tracheal preparations (Ach 1 x 10(-9)-1 x 10(-4) g ml-1) and disappeared in vivo when the animals were sensitized with ovalbumin (OA, 100 mg kg-1 i.p. + 100 mg kg-1 s.c.). The hyporesponsiveness was also absent in ovalbumin sensitized guinea-pigs exposed to an aerosol of ovalbumin 60 min before testing with Ach. 3. In non-sensitized guinea-pigs, pretreatment with butoxamine (1 mg kg-1 i.v.) or with theophylline (25 mg kg-1 i.v.), completely abolished the effect of noise-exposure. In contrast, pretreatment with L-NG-nitro-arginine methyl ester (L-NAME, 10 mg kg-1 i.v.), alpha-chymotrypsin (2 U kg-1 i.v.) or with enprofylline (10 mg kg-1 i.v.), did not affect it. 4. In conclusion, our experiments reveal inhibitory mechanisms upon Ach-induced bronchoconstriction activated by a stress stimulus and this is absent in sensitized animals. These mechanisms seem to be linked to the adrenergic beta 2-receptors and a role for the purinergic system (via A-receptors) may also be present.

Acetylcholine↗
PubMed1983

Additional evidence against universal modulation of beta-adrenoceptor responses by excessive thyroxine.

1 The effect of prolonged, excessive thyroxine on beta-adrenoceptor-mediated relaxation of guinea-pig trachea was studied. 2 Thyroxine did not significantly affect the potency of the beta 1-adrenoceptor agonist, noradrenaline, or the beta 2-adrenoceptor agonist, terbutaline. 3 Thyroxine did not significantly affect the apparent KB values of the selective beta 1-adrenoceptor antagonist, practolol, or the selective beta 2-adrenoceptor antagonist, butoxamine. 4 Thyroxine did not significantly affect the maximum response to noradrenaline. The maximum response to terbutaline in tissues from the thyroxine-treated animals was only slightly lower than the maximum response in tissues from paired control animals. 5 These results suggest that excessive thyroxine does not significantly affect the beta-adrenoceptor-mediated relaxation of guinea-pig trachea and that the reported modulation of beta-adrenoceptor-mediated responses in other tissues is specific for the given tissue rather than common to all beta-adrenoceptor systems.

Animals↗
PubMed1982

Pharmacological isolation of a single beta-adrenoceptor subtype makes Schild plots which have slopes of 1 possible for selective beta-adrenoceptor antagonists in carbachol-contracted guinea-pig trachea.

The effects of selective beta-adrenoceptor agonists and antagonists on isometric relaxation of carbachol-contracted, guinea-pig isolated trachea were studied. An attempt was made to pharmacologically isolate the beta 1- and beta 2-adrenoceptors by use of appropriate selective agonists and antagonists. The slopes of the Schild plots for butoxamine vs noradrenaline and terbutaline as well as for practolol vs terbutaline did not differ significantly from 1, the predicted value for a competitive antagonist acting at a single receptor type. These data differ from a previous report suggesting that slopes of less than 1 are characteristic for selective beta-adrenoceptor antagonists in carbachol-contracted guinea-pig trachea. They support the hypothesis that the slopes in this preparation are due to interaction of the agonist with both beta 1- and beta 2-adrenoceptors rather than the state of contraction of the trachea.

Adrenergic beta-Antagonists↗
PubMed1996

The effect of distension of the stomach on peripheral blood flow in anaesthetized pigs.

The present study was undertaken in anaesthetized pigs to determine the primary reflex effects of gastric distension on the peripheral circulation. Changes in blood flow in the splenic, superior mesenteric, left renal and left external iliac arteries were assessed using electromagnetic flowmeters during distension of a balloon in the stomach, performed at constant aortic blood pressure and heart rate, with 0.6 l of Ringer solution (mean gastric transmural pressure of about 12 mmHg). In fourteen pigs, a decrease in splenic, renal and iliac flows and variable changes in mesenteric flow were obtained. A decrease in mesenteric flow and more marked decreases in the other flows occurred in response to the distension after the administration of propranolol or butoxamine. In five pigs, the vasoconstrictive responses were graded by step increments in gastric distending volume from 0.4 to 0.8 l. The above responses were abolished by the administration of phentolamine (eight pigs) and by bilateral cervical vagotomy (six pigs). The results showed that innocuous distension of the stomach in anaesthetized pigs reflexly caused vasoconstriction in the splenic, renal and iliac vascular beds; vasoconstriction also occurred in the mesenteric vascular bed but only after beta-blockade. These reflex responses were mediated by sympathetic mechanisms which involved both alpha and beta vascular adrenoceptors and their afferent limb was in the vagal nerves.

Analysis of Variance↗
PubMed1978

Mediation of isoproterenol-induced thirst in rats by beta2-adrenergic receptors.

Isoproterenol-induced thirst in rats has been attributed to the activation of beta-adrenergic receptors. Since these receptors can be further differentiated pharmacologically into beta1 and beta2 types, experiments were performed using several beta-adrenergic agonists and antagonists to determine the receptor type initiating the isoproterenol-induced thirst. The beta1- and beta2-adrenergic antagonist, d,l-propranolol (1 mg/kg, ip), blocked the increase in water intake usually accompanying acute subcutaneous administration of isoproterenol (25 microgram/kg) to female rats. Since l-propranolol is known to stabilize membranes and to possess anesthetic-like properties, d-propranolol was also used. This isomer has little beta-adrenergic-blocking activity but possesses anesthetic-like activity. Administration of d-propranolol (1 mg/kg, ip) failed to affect the drinking response to acute administration of isoproterenol (25 microgram/kg). Practolol (125 mg/kg), a beta1-adrenergic antagonist with little anesthetic properties, also had no effect on water intake of isoproterenol-treated rats. Butoxamine, a selective beta2-adrenergic antagonist, attenuated the drinking response to isoproterenol. Salbutamol (150 microgram/kg), a beta2-adrenergic agonist, mimicked the effect of isoproterenol on water intake. These results are consistent with the suggestion that beta2-adrenergic receptors mediate the isoproterenol-induced thirst in rats.

Albuterol↗