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PubMedDate not supplied

Beta-adrenoceptors in the detrusor of guinea pig bladder.

In the present study, we tried to determine which beta-adrenoceptor subtypes are involved in the inhibitory regulation of bladder motility in the guinea pig by using in vitro functional analysis. Isoprenaline, norepinephrine and epinephrine decreased spontaneous contractile activity of the bladder concentration-dependently, the rank order of their potency being isoprenaline (pD2 = 7.38)>norepinephrine (6.71)>epinephrine (6.31). Dobutamine was also effective in inhibiting the spontaneous contraction (5.81). However, CGP-12177, BRL37344, salbutamol, and clenbuterol were not effective at the concentration of 30 microM. The concentration response curves of catecholamines (isoprenaline, norepinephrine and epinephrine) were rightward shifted by the presence of atenolol. Schild regression analyses carried out for atenolol against isoprenaline, norepinephrine and epinephrine gave pA2 values of 6.93, 6.78 and 6.69, respectively. The concentration-response curve for isoprenaline was unaffected by 10 microM butoxamine. In the presence of 1 microM propranolol, bupranolol produced shifts of the concentration-response curve for isoprenaline, and the apparent pA2 value for bupranolol against isoprenaline was 5.50. These results suggest that the inhibition of spontaneous contraction of the guinea pig bladder by beta-adrenoceptor agonists is mediated mainly via beta1-adrenoceptor and the effect of isoprenaline is mediated partly via atypical beta-adrenoceptor subtype.

Adrenergic beta-Agonists↗
PubMed2003

MaxiK channel mediates beta2-adrenoceptor-activated relaxation to isoprenaline through cAMP-dependent and -independent mechanisms in guinea-pig tracheal smooth muscle.

We examined the contribution of large-conductance, Ca(2+)-sensitive K+ (MaxiK) channel to beta2-adrenoceptor-activated relaxation to isoprenaline in guinea-pig tracheal smooth muscle focusing on the role for cAMP in the coupling between beta2-adrenoceptor and MaxiK channel. Isoprenaline-elicited relaxation was confirmed to be mediated through beta2-type of adrenoceptor since the response was antagonized in a competitive fashion by a beta2-selective adrenoceptor antagonist butoxamine with a pA2 value of 6.56. Isoprenaline-induced relaxation was significantly potentiated by a selective inhibitor of cyclic AMP-specific phosphodiesterase, Ro-20-1724 (0.1-1 microM). cAMP-dependent mediation of MaxiK channel in the relaxant response to isoprenaline was evidenced since the potentiated response to isoprenaline by the presence of Ro-20-1724 (1 microM) was inhibited by the channel selective blocker, iberiotoxin (IbTx, 100 nM). This concept was supported by the finding that the relaxation to a membrane permeable cAMP analogue, 8-bromo-cAMP (1 mM), was susceptible to the inhibition by IbTx. On the other hand, isoprenaline-induced relaxation was not practically diminished by an adenylyl cyclase inhibitor SQ 22,536 (100 microM). However, isoprenaline-induced relaxation in the presence of SQ 22,536 was suppressed by IbTx. Characteristics of isoprenaline-induced relaxant response, i.e., impervious to SQ 22,536 but susceptible to IbTx, were practically mimicked by cholera toxin (CTX, 5 microg/ml), an activator of adenylyl cyclase coupled-heterotrimeric guanine nucleotide-binding regulatory protein Gs. These findings indicate that in guinea-pig tracheal smooth muscle: 1) MaxiK channel substantially mediates beta2-adrenoceptor-activated relaxation; 2) both cAMP-dependent and -independent mechanisms underlie the functional coupling between beta2-adrenoceptor and MaxiK channel to induce muscle relaxation; and 3) direct regulation of MaxiK channel by Gs operates in cAMP-independent coupling between beta2-adrenoceptor and this ion channel.

Adrenergic beta-Agonists↗
PubMed1999

Evidence for beta3-adrenoceptor subtypes in relaxation of the human urinary bladder detrusor: analysis by molecular biological and pharmacological methods.

The purpose of the present study was to confirm the presence of beta3-adrenoceptor subtype in the relaxation of human urinary bladder detrusor tissue by reverse transcription-polymerase chain reaction (PCR); direct sequencing of the PCR product, in situ hybridization; and isometric contraction. Using reverse transcription-PCR, the mRNAs of three receptor subtypes (beta1, beta2, and beta3) were expressed in the human urinary bladder detrusor tissue. Direct sequencing of the PCR product of the above beta3-adrenoceptor revealed no mutation in the amplified regions. In situ hybridization with digoxygenin-labeled oligonucleotide probe revealed the presence of the mRNA of beta3-adrenoceptor subtype in the smooth muscle of the urinary bladder. The relaxant effects of isoproterenol (a nonselective beta-adrenoceptor agonist); ZD7114, BRL37344, and CGP12177A (putative selective beta3-adrenoceptor agonists); and SR59230A (a putative selective beta3-adrenoceptor antagonist) were tested using an isometric contraction technique. Isoproterenol in either the presence or absence of both atenolol (a beta1-adrenoceptor-selective antagonist) and butoxamine (a beta2-adrenoceptor-selective antagonist) revealed a relaxant effect on the carbachol-induced contraction of the human urinary bladder detrusor. Both BRL37344 and CGP12177A also revealed relaxant effects on the human urinary bladder detrusor, but ZD7114 did not elicit any relaxation. These results suggest that beta3-adrenoceptor may have some role in urine storage in the human urinary bladder.

Adrenergic beta-Agonists↗
PubMed1964

[REVIEW OF PSYCHODYSLEPTICS: I. CLASSIFICATION OF PSYCHODYSLEPTICS].

The discovery of new dysleptic drugs has prompted the present review of these substances which influence neuropsychic activity. It is possible to divide dysleptics into two categories: under the first heading fall mescaline, LSD-25, psilocybine, adrenochrome, bufotenine and dimethyltryptamin; the other group includes Ditran, Butoxamine, WH-4849, and AHR-379. The place of Sernyl could not be ascertained and it might well constitute a class by itself. The mescaline type of reaction is mainly characterized by the induction of perceptual distortions without alteration of the state of consciousness, whereas the Ditran type reaction is one of confusion with postexperimental amnesia. Electroencephalographic recordings support this classification: lowering of amplitude, acceleration of rhythm and desynchronization were noted with the first group; and slowing of rhythm and slow waves similar to those seen during the onset of sleep, with the other group.

Adrenochrome↗
PubMed1977

Differential inhibition of lipolysis in human adipose tissue by adrenergic beta receptor blocking drugs.

The effects of various adrenergic beta receptor agonists and antagonists on lipolysis (measured as glycerol release) in human adipose tissue in vitro were studied. Of the agonists investigated, the potency rank order was isoproteronol greater than norepinephrine greater than salbutamol. Adrenergic beta receptor blocking drugs inhibited catecholamineinduced lipolysis competitively. Propranolol was the overall most effective compound, followed by metoprolol, alprenolol and practolol, whereas butoxamine and H35/25 were weak inhibitors. The results indicate that the adrenergic reciptor mediating lipolysis in human adipose tissue is of type beta-1. Basal and theophylline-induced lipolysis was reduced when higher concentrations of these drug were used.

Adipose Tissue↗
PubMed2006

Histological evidences of reparative and regenerative effects of beta-adrenoceptor agonists, clenbuterol and isoproterenol, in denervated rat skeletal muscle.

The aim of this study was to determine the contribution of beta-adrenoceptor activation in the reconstruction of the structural and functional organization of denervated skeletal muscle. beta-agonists, clenbuterol (1.2 mg/kg body weight) and isoproterenol (2 mg/kg body weight), administration (daily oral administration; maximum 7 days) to normal innervated rats as well as denervated animals caused muscle hypertrophy. An increase in mean fiber diameter confirmed this stimulated growth both in normal innervated and denervated rat gastrocnemius muscle. Examination of muscle nuclei from treated but normal innervated rat gastrocnemius exhibited features like large size, active nucleoplasm and an increase in their number per fiber cross section and per mm mean fiber length indicating towards an elevated biosynthetic activity in tissue in the presence of beta adrenoceptor agonists. Administration of drugs to normal innervated animals resulted in an emergence of central muscle nuclei. The hyperactive and enlarged muscle nuclei ultimately organized themselves into unusually elongated nuclear streaks. beta agonist treatment to denervated rats resulted in amelioration of atrophic state of tissue characterized by hypertrophy of muscle fibers thus lending to a restoration of structural organization of tissue. Bizarre shapes of nuclei in denervated muscle tend to recover to that characteristic to normal innervated muscle in presence of clenbuterol and isoproterenol hydrochloride. All observations were confirmed by administering butoxamine, a beta-adrenoceptor antagonist along with beta-agonists. The results suggests that both clenbuterol and isoproterenol hydrochloride are capable of mimicking normal innervation functions in skeletal muscle and thus play important role in the structural and functional reorganization of tissue. Amelioration of denervation atrophy in rat gastrocnemius in the presence of beta-agonists supports this.

Adrenergic beta-Agonists↗
PubMed2006

Isoproterenol ameliorates workstress-induced rat skeletal muscle degeneration.

Beta-Agonists though have been widely studied for their protein anabolic effects in skeletal muscles, but the lipid status under work stress and agonist treatment have not been understood well in the skeletal muscles and heart of rat. In the present study, adult male Wistar rats were subjected to work overload stress and beta agonist isoproterenol treatment (2 mg kg(-1) day(-1) intraperitoneally) to examine, whether it attenuates work stress-induced changes or not. Simultaneously, beta2 antagonist butoxamine (2 mg kg(-1) day(-1) intraperitoneally) was administered to another isoproterenol-treated group. Work stress led to myofibrillar degeneration as well as rapid utilization of lipid to meet increased energy demands and for muscle repair, which was reflected through histochemical localization of lipids and biochemical estimation of cholesterol and triglycerides. Significantly decreased cholesterol levels in skeletal muscles and heart muscles were noticed. As expected, isoproterenol reversed the conditions by raising cholesterol and triglyceride levels significantly in the skeletal muscles and also by ameliorating the degenerative changes in muscle fibres as induced by work overload. However, severe accumulation of lipids in heart infers towards deleterious effects of isoproterenol on heart and thus remains a limiting factor for its immediate clinical application. Further research is needed to separate desirable effects of beta agonists on skeletal muscles from any undesirable effects on the heart, so as to optimize their therapeutic potential.

Adrenergic beta-Agonists↗
PubMed1990

Centrally mediated alpha & beta adrenoceptors controlling blood pressure in rabbits.

The effect of intracerebroventricular (icv) injection of noradrenaline (NA) on the blood pressure was studied in anaesthetised rabbits. Adrenoceptor blockers were used to study the specific adrenoceptor mediating the response. The results indicated a hypotensive response to icv injection of NA. This hypotensive response to NA was blocked by alpha-2 (yohimbine) and beta-1 (metoprolol) but not by alpha-1 (prazosin) and beta-2 (butoxamine) adrenoceptor blockers.

Adrenergic alpha-Antagonists↗
PubMed1977

The effect of beta-adrenoceptor antagonists on the alpha-adrenoceptor blockade produced by phenoxybenzamine.

The effect of beta-adrenoceptor antagonists on the irreversible alpha-adrenoceptor blockade produced by phenoxybenzamine was studied in dogs. The pressor effects of adrenaline were revived after the inhibition by the alpha-receptor block by (+/-) propranolol, (-) INPEA, (+/-) MJ 1999 and (+/-) butoxamine. The enantiomers (+) propranolol and (+) INPEA were ineffective in this regard. (+/-) Practolol also did not revive the pressor effect of the amines. The alpha-receptor mediated effect of the amines, in the nictitating membrana-receptor blockade. It is concluded that (1) blockade of the peripheral (beta-2) receptors is essential for the revival of the pressor effects, (2) local anesthetic effect of the beta-antagonists is not involved. Further work using a series of doses of agonists and antagonists of alpha-and beta-receptors is indicated to clarify the nature of this drug-interaction.

Adrenergic beta-Antagonists↗
PubMed1990

Alpha 1-adrenergic stimulation and beta 2-adrenergic inhibition of DNA synthesis in vascular smooth muscle cells.

Effects of catecholamines on DNA synthesis in vascular smooth muscle cells (VSMC) were investigated in a chemically defined medium that included insulin, transferrin, and sodium selenite. Smooth muscle-rich preparation was obtained from rat aortic media and VSMC were further purified by cell cloning. A clone that was positive for smooth muscle actin and was negative for the coagulation factor VIII was used in this study. The fetal calf serum-induced proliferation was enhanced by alpha-adrenergic and inhibited by beta-adrenergic stimulation. When cells of low passages were used, dose-response curves for norepinephrine were biphasic; when cells were subconfluent, norepinephrine stimulated DNA synthesis at as low as 1 nM and was apparently ineffective at more than 100 nM. When cells were confluent, the effect of norepinephrine was inhibitory at lower concentrations (less than 1 nM) and stimulatory at relatively higher concentrations. Cells of higher passages exhibited only inhibitory effects of the amine. Stimulatory and inhibitory effects on DNA synthesis were mediated through alpha 1- and beta 2-adrenergic receptors, respectively. Thus, the alpha 1-agonist phenylephrine was more potent than the alpha 2-agonist clonidine in stimulating DNA synthesis. An alpha 1-adrenergic antagonist, prazosin, was more effective than the alpha 2-adrenergic antagonist yohimbine in antagonizing the stimulatory effect of norepinephrine. beta-Adrenergic agonists inhibited DNA synthesis with IC50 values in the nanomolar range; the rank order of potency of agonists was isoproterenol greater than salbutamol greater than or equal to (-)-epinephrine much greater than (-)-norepinephrine, consistent with beta 2-receptor specificity. (+)-Epinephrine or (+)-norepinephrine, the stereoisomers of the catecholamines, were ineffective. The inhibitory effects of norepinephrine were reversed by beta-adrenergic antagonists, with the rank order of potency of pindolol greater than butoxamine greater than atenolol, consistent with beta 2-receptor specificity. The dose-response curves of norepinephrine, therefore, seemed to be determined by a balance between alpha 1-receptor-mediated stimulation and beta 2-receptor-mediated inhibition of DNA synthesis. Minimum time required for exhibiting alpha 1-adrenergic or beta 2-adrenergic effects was between 6 and 15 hr, suggesting that the G0 or G1 phase of the cell cycle might be the site of action. These results show that catecholamines dually modulate DNA synthesis in VSMC through specific adrenergic receptors.

Animals↗
PubMed1975

[The calorigenic effect of glucagon].

The calorigenic action of glucagon was studied in several species by measuring its effect on the oxygen comsumption. The calorigenic effect was most pronounced in the quail and also evident in young adult rats of two different strains but not in mice and guinea pigs. The influence of various drugs on the calorigenic effect of glucagon was investigated in rats. Ganglionic blocking agents (hexamethonium, mecamylamine, chlorisondamine) as well as adrenergic blocking drugs (propranolol, butoxamine, phentolamine) greatly reduced the glucagon-induced calorigenesis but after pretreatment with reserpine, guanethidine or chemical sympathectomy with 6-hydroxydopamine the calorigenic effect of glucagon was exaggerated. It was somewhat diminished by nicotinic acid but not by chlorpromazine or lithium and potentiated by cocaine but not by theophylline.--These results are not indicative for an involvement of adenly cyclase--cyclic AMP--system in glucagon-induced calorigenesis but they are compatible with the assumption that the hormone enhances the metabolic rate by releasing catecholamines from the adrenal medulla.

Animals↗
PubMed1987

Alpha- and beta-adrenergic receptors in the horse ureter.

The presence of both alpha and beta adrenergic receptors in the caudal third ureter of the horse were studied in vitro under isometric conditions using adrenergic agonist and antagonist drugs. Isoprenaline and the beta 2- stimulating agent, salbutamol, elicited relaxation of the ureter smooth muscle strips. The responses were not affected by the beta 1- blocking agent, practolol, but were totally abolished by propranolol and the beta 2- blocking agent, butoxamine. The stimulation of alpha-adrenergic receptors with noradrenaline and phenylephrine evoked a contractile effect which was totally inhibited by phenoxybenzamine and the alpha 1- blocking agent, prazosin. It is concluded that in the horse ureter the alpha receptors are dominant and belong to alpha 1 subtype while the beta receptors are recessive and belong to beta 2- adrenoceptor subtype.

Animals↗
PubMed1985

Differential inhibition of beta adrenergic receptors in human and rabbit ciliary process and heart.

Prior biochemical studies have suggested that beta adrenergic receptors in the ciliary process are mostly of the beta-2 subtype. The present experiments evaluate a number of beta adrenergic antagonists, including several recently developed drugs, for their ability to block rabbit and human ciliary process and heart beta adrenergic receptors activating adenylate cyclase. Three of these agents (alpha-methylpropranolol, IPS 339 and ICI 118,551) demonstrated a high degree of oculoselectivity in both rabbit and human. The other agents (S 37-429, S 32-468, ICI 78,462,H35/25, butoxamine, propranolol, timolol, atenolol and practolol) showed either modest or no oculoselectivity. Structure-activity studies suggested that, among antagonists of the aryloxymethyl type, methylation of the side-chain alpha-carbon or the aromatic ring may enhance oculoselectivity primarily by decreasing potency at cardiac beta adrenergic receptors. Additional physiological studies of cardiac chronotropic response revealed that, compared with nonselective beta blockers, compounds with biochemical oculoselectivity demonstrate decreased physiological effects on cardiac function. This was true when the selective agents were applied either systemically or topically to the eye. On the other hand, the systemic absorption of topical timolol was sufficient to block cardiac chronotropic effects completely. These findings, identifying relatively specific blockers of rabbit and human ciliary process beta adrenergic receptors, have implications for the development of ocular hypotensive agents with fewer systemic side effects on tissues enriched in beta-1 adrenergic receptors.

Adenylyl Cyclases↗
PubMed1986

Ablation of the myenteric plexus impairs alpha but not beta adrenergic receptor-mediated mechanical responses of rat jejunal longitudinal muscle.

The mechanical responses produced by alpha and beta adrenergic receptor agonists were evaluated in control and myenteric neuron-ablated rat jejunal longitudinal muscle. The myenteric plexus of the jejunum was destroyed by serosal application of benzalkonium chloride (BAC). The beta adrenergic receptor agonists isoproterenol and sulfonterol produced a concentration-dependent relaxation of both control and BAC-treated jejunum. Dose-response curves obtained in control and BAC-treated jejunum were nearly superimposable regardless of the beta agonist used. Isoproterenol-induced relaxation was antagonized by the beta receptor antagonists propranolol and practolol but not by butoxamine. The alpha-1 selective agonists phenylephrine and methoxamine were more potent and efficacious in producing relaxation of control than BAC-treated jejunum. The relaxant responses of methoxamine and phenylephrine in control jejunum were blocked by prazosin but not by yohimbine. The supposed alpha-2 selective agonist clonidine also produced a concentration-dependent, prazosin-sensitive, yohimbine-resistant relaxation which was markedly greater in control than BAC-treated jejunum, consistent with alpha-1 receptor stimulation. Clonidine tested in the presence of prazosin and the alpha-2 selective receptor agonists UK-14,304, M-7 and B-HT 920 all produced a concentration-dependent contraction of control but not BAC-treated jejunum. The contractile response produced by UK-14,304 was antagonized by yohimbine but not by atropine. Our results suggest that in rat jejunal longitudinal muscle: beta adrenergic receptors mediate relaxation and are located on the smooth muscle; alpha-1 adrenergic receptors mediate relaxation and are located on both the smooth muscle and myenteric plexus.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1986

[A study on the renal action of beta 1- and beta 2-adrenoceptors in rats].

The present experiments were designed to study urine volume and urinary sodium excretion effects of beta-antagonists and beta-agonists with reference to beta 1- and beta 2-adrenoceptors in rats. The beta-antagonists used were atenolol as a selective beta 1-antagonist, butoxamine as a beta 2-antagonist and propranolol as a non-selective beta-antagonist. The beta-agonist used were salbutamol as a beta 2-agonist and isoproterenol as a non-selective beta-agonist. Beta-antagonists increased the urine volume and urinary sodium excretion, but beta-agonists decreased the urine volume and urinary sodium excretion. With regards to these effects, atenolol increased the urine volume more than urinary sodium excretion, isoproterenol decreased the urine volume more than urinary sodium excretion, and salbutamol decreased the urinary sodium excretion more than urine volume. When beta-antagonists were infused with a beta-agonist, the original diuretic effects of these beta-antagonists were inhibited by the beta-agonist. In these effects, beta-antagonists infused with isoproterenol inhibited urine volume more than urinary sodium excretion, but beta-antagonists infused with salbutamol inhibited urinary sodium excretion more than urine volume. These results indicate that the urine volume is related to beta 1-adrenoceptors, while the urinary sodium excretion is related to beta 2-adrenoceptors, although there is no selectivity towards either beta 1-adrenoceptors or beta 2-adrenoceptors as far as diuresis or antidiuresis is concerned.

Adrenergic beta-Agonists↗
PubMed1987

Effects of footshock stress on the sensitivity of the isolated rat pacemaker to catecholamines.

The effect of repeated footshock on the sensitivity of the isolated rat pacemaker to the chronotropic effect of catecholamines was studied. Footshock stress caused subsensitivity to noradrenaline and supersensitivity to isoprenaline. The subsensitivity to the neurotransmitter was abolished by cocaine, whereas supersensitivity to isoprenaline was unchanged after blockade of the extraneuronal uptake. The pA2 value of metoprolol was increased by repeated footshock. Butoxamine reversed the supersensitivity to isoprenaline and the alteration of the pA2 value. Repeated footshock stress appears to cause prejunctional subsensitivity to noradrenaline and to increase the function of postjunctional beta 2-adrenoceptors.

Adrenergic beta-Antagonists↗
PubMed1988

Effects of alpha- and beta-adrenergic agonists on Trypanosoma cruzi interaction with host cells.

We studied the effects of adrenergic agonists on the capacity of blood trypomastigote forms of Trypanosoma cruzi to associate with (i.e., bind and/or penetrate) host cells in vitro. The extent of T. cruzi association with mouse macrophages in the presence of the beta-adrenergic agonist L-isoproterenol was significantly decreased with respect to mock-treated controls. Similar results were obtained when the parasite was pretreated with L-isoproterenol and was then allowed to interact with untreated macrophages. In contrast, pretreatment of trypomastigotes with either L-phenylephrine or methoxamine-alpha-adrenergic agonists--enhanced their reactivity with macrophages. Interaction with a nonphagocytic host cell was also decreased and increased by parasite pretreatment with beta- and alpha-adrenergic agonists, respectively. The L-isoproterenol and L-phenylephrine effects were no longer detectable 2 and 3 hr after their removal, respectively, and were therefore reversible. Atenolol, a specific beta 1 adrenoreceptor blocker inhibited the L-isoproterenol effect, whereas butoxamine, a specific beta 2 blocker, did not. Thus, beta 1-like but not beta 2-like binding sites appeared to be expressed on T. cruzi. Both prazosin and yohimbine, preferential alpha 1- and alpha 2-receptor blockers, respectively, abolished the L-phenylephrine effect. The opposite effects of alpha- and beta-adrenergic agonists suggested that the infectivity of T. cruzi may be regulated by activation of surface components comparable to the adreno-receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1988

Influence of the autonomic nervous system in the horse urinary bladder.

alpha and beta-adrenergic receptors in detrusor muscle and bladder base of horses were investigated by in vitro responses of smooth muscle strips to exogenous agonist and antagonist drugs. Noradrenaline, isoprenaline and salbutamol induced relaxation of detrusor muscle strips which was significantly inhibited by propranolol and butoxamine suggesting that the response is mediated by beta-2 adrenergic receptors. In the urinary bladder base noradrenaline, phenylephrine and B-HT 920 induced strong contractile effects. These contractile responses were inhibited by the alpha antagonist phenoxybenzamine, the alpha-1 selective antagonist prazosin and the alpha-2 selective antagonist yohimbine. The inhibitory action of prazosin was more potent than that observed with yohimbine suggesting that the response in the bladder base of horses is mediated predominantly by alpha-1 adrenergic receptors, although alpha-2 receptors also participate.

Adrenergic alpha-Agonists↗