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PubMed1983

The selectivity of beta-adrenoceptor antagonists on isoprenaline-induced changes in heart rate, blood pressure, soleus muscle contractility and airways function in anaesthetized cats.

The beta-adrenoceptor antagonist of propranolol, metoprolol, atenolol and butoxamine in anaesthetized cats has been measured and compared with the activity of four synthetic phenylethanolamine derivatives. The effects of isoprenaline on four parameters in the anaesthetized cat: heart rate, blood pressure, soleus muscle contractility and airway reactance, were measured and the modification of the isoprenaline dose-response relation by each of the antagonist drugs assessed. Parallel shifts in log dose-response curves for isoprenaline were caused by propranolol for all parameters, by metoprolol and atenolol for each parameter except blood pressure, and butoxamine for each except soleus muscle and heart rate. Selectivity of action of the antagonists between different organs was measured by comparing DR10 values, computed from isoprenaline dose-ratios. Propranolol was the most potent antagonist and showed slight selectivity of action on soleus muscle compared with heart. Atenolol and metoprolol were approximately equipotent and were cardioselective at low doses only. Butoxamine was the least potent antagonist and possessed non-beta-adrenoceptor effects on the parameters measured. Each of the new compounds, 4'-bromo-2'-methoxy-N-isopropyl phenylethanolamine, the 4'-chloro- and 4'-methyl analogues, and 4'-methoxy-N-t-butyl phenylethanolamine, was a potent antagonist but did not exhibit any selectivity of action. The results suggest no clear separation of beta-adrenoceptors into beta 1- and beta 2-subclasses in organs of the cat. There is no apparent separation of beta-adrenoceptor-mediated effects on skeletal muscle and airways.

Adrenergic beta-Antagonists↗
PubMed1983

Difference between adrenergic beta 1- and beta 2-blocking effects on isoproterenol-induced Ca spike suppression in guinea-pig taenia coli.

Ca spike suppressions induced by isoproterenol (IsP) and a beta 2-agonist, 5-hydroxymethyl-6-hydroxy-2-isopropylamino-1,2,3,4-tetrahydronaphthalene -1-ol (AA497), were investigated in the presence of butoxamine or practolol. The relaxations were isotonically recorded, and the Ca spike frequency was recorded using the single sucrose gap method. IsP-induced relaxation was not inhibited by butoxamine (Butox, 0.16 microM), but was inhibited by practolol (Prac, 0.188 microM). In 24 mM K+-Krebs' solution, AA497 caused relaxation in a lower dose range and suppressed to a small extent the Ca spike frequency in a higher dose range, as was observed for IsP-induced curves of log dose-spike frequency and log dose-relaxation. In normal K+-Krebs' solution, both IsP and AA497 greatly suppressed the Ca spike frequency. IsP (1.21 microM)-induced suppression of the Ca spike frequency was blocked by Prac (113 microM), and it was blocked by Butox (96 microM) to a greater extent. AA497-induced suppression of the spikes was not blocked by Prac (37.6 microM), but completely blocked by Butox (32 microM). These selective inhibitory effects of butoxamine on AA497-induced and IsP-induced Ca spike suppression demonstrate that in the adrenergic beta-receptor-mediated process in taenia coli, beta 2-mechanisms are more closely related to the Ca spike suppression than the beta 1-mechanisms are.

Adrenergic beta-Antagonists↗
PubMed2002

The beta2- and beta3-adrenoceptor-mediated relaxation induced by fenoterol in guinea pig taenia caecum.

Fenoterol, a beta2-adrenoceptor selective agonist, belongs to the arylethanolamine class. To understand the receptor subtypes responsible for beta-adrenoceptor-mediated relaxation of guinea pig taenia caecum, we investigated the effect of fenoterol. Fenoterol caused concentration-dependent relaxation of the guinea pig taenia caecum. Propranolol, bupranolol and butoxamine produced shifts of the concentration-response curve for fenoterol. Schild regression analyses carried out for propranolol, butoxamine and bupranolol against fenoterol gave pA2 values of 8.41, 6.33 and 8.44, respectively. However, in the presence of 3 x 10(-4) M atenolol, 10(-4) M butoxamine and 10(-6) M phentolamine to block the beta1-, beta2- and a-adrenoceptor effects, respectively, Schild regression analysis carried out for bupranolol against fenoterol gave pA2 values of 5.80. These results suggest that the relaxant response to fenoterol in the guinea pig taenia caecum is mediated by both the beta2- and the beta3-adrenoceptors.

Adrenergic beta-Agonists↗
PubMed1975

Effects of beta adrenergic blocking agents on erythropoietin production in rabbits exposed to hypoxia.

The effects of dl-propranolol, d-propranolol, butoxamine or practolol on erythropoietin (ESF) production in rabbits exposed to hypoxia (0.42 atmosphere) for 18 hours were investigated. Rabbits treated with dl-propranolol (4 or 8 mg/kg i.p.) or butoxamine (15 or 30 mg/kg i.p.) produced significantly less ESF in response to hypoxia than did saline-treated control animals. ESF production in rabbits given d-propranolol or practolol during hypoxia was not significantly different from that of control animals exposed to hypoxia. Based on the proposed selectivity of butoxamine for beta2 adrenergic receptors and of practolol for beta1 adrenergic receptors, it is suggested that ESF production in rabbits exposed to hypoxia may involve the activation of beta2 adrenergic receptors.

Adrenergic beta-Antagonists↗
PubMed1986

Bovine anterior descending coronary artery possesses a homogeneous population of beta-1 adrenergic receptors.

Isolated vessel rings from the proximal and distal ends of the bovine anterior descending coronary artery were mounted in tissue baths for the measurement of isometric contraction. These rings were pre-exposed to phenoxybenzamine to block tissue catecholamine uptake and alpha adrenoceptors. They were then contracted with high potassium, and beta adrenergic agonist dose-relaxation response curves were obtained in the presence and absence of beta antagonists. The orders of agonist potency in the arterial rings were the same as that in spontaneously beating guinea pig atria: isoproterenol (ISO) greater than norepinephrine (NE) greater than fenoterol (FE) greater than salbutamol (SA) and differed from that in the guinea pig trachea: ISO greater than FE greater than SA greater than NE. Schild analysis yielded propranolol pA2 values in the coronary artery rings which did not differ between the four agonists studied or between the proximal and distal ends of the coronary artery. Similar results were obtained with practolol and butoxamine with the exception that in the case of butoxamine, a higher pA2 value was obtained against ISO in the distal ring preparations. The practolol and butoxamine pA2 values in the artery rings matched the respective--log KB values obtained in the guinea pig atria using NE as the agonist but were the reverse of those obtained in the guinea pig trachea using either FE or SA as the agonist. It is concluded that the proximal and distal ends of the bovine anterior descending coronary artery possess a homogeneous population of beta-1 adrenergic receptors.

Adrenergic beta-Agonists↗
PubMed1984

Extrarenal potassium transport and the beta 2-adrenergic system.

The distribution of a short-term potassium load was quantitated in three groups of acutely nephrectomized rats infused with KCl at 0.75, 1.50, and 2.25 mEq/kg/hr for 90 minutes. The rate of net potassium transfer from the extracellular fluid compartment to the intracellular fluid compartment was stable from 30 to 90 minutes and proportional to the rate of infusion, with no evidence of saturation of transport mechanisms. In the period 60 to 90 minutes, the calculated increments in intracellular potassium concentration over 10-minute intervals were similar to the respective increments in extracellular potassium concentration. The apparent volume of distribution of the infused potassium over this period was similar to total body water. At the termination of the infusions, the net potassium transfer rates rapidly fell to very low levels. Our studies support the view that the extrarenal modulation of short-term potassium load is dependent on changes in plasma potassium concentration that conform to a first-order linear kinetic model. The infusion of the selective beta 2-adrenergic blocker butoxamine without potassium administration to acutely nephrectomized rats resulted in a net efflux of potassium from the intracellular fluid compartment. The addition of butoxamine to three groups of rats receiving KCl at the previous rates resulted in a fixed decrement in net potassium transfer to the intracellular fluid compartment that was not significantly different from the net efflux of potassium seen with butoxamine alone. Despite beta blockade, the net transfer of potassium remained proportional to the infusion rate. Thus, in our studies, beta 2-adrenergic blockade had a relatively fixed influence on decreasing net potassium transfer, both under basal conditions and during short-term potassium administration.

Adrenergic beta-Antagonists↗
PubMed1981

Beta-1 receptor mediation of renin secretion elicited by low-frequency renal nerve stimulation.

The purpose of this study was to determine if renin secretion resulting solely from low-frequency renal nerve stimulation (no change in renal blood flow or urinary sodium excretion) is mediated by activation of beta-1 (beta-1) or beta-2 (beta-2) adrenergic receptors. Beta-1 and beta-2 adrenergic receptor blockade were produced with atenolol and butoxamine, respectively. Low-frequency renal nerve stimulation (0.5 Hz) increased renin secretion without altering mean arterial pressure, renal blood flow, glomerular filtration rate or urinary sodium excretion. The increase in renin secretion in response to renal nerve stimulation was blocked by beta-1 blockade with intrarenal atenolol (2.0 micrograms/kg/min) infusion. This dose of atenolol reduced the renal vasodilator response to intrarenal isoproterenol by only 48%, thus indicating modest beta-2 receptor blockade. A lower dose of atenolol (30 micrograms/kg i.v.) markedly decreased the tachycardia in response to i.v. isoproterenol (2 micrograms) but had no effect on the renal vasodilator response to intrarenal isoproterenol injection (2 micrograms), thus indicating selective beta-1 blockade. This dose of atenolol abolished the increase in renin secretion during renal nerve stimulation. In contrast, beta-2 receptor blockade with butoxamine (20 micrograms/kg/min) did not alter the renin secretion response to renal nerve stimulation. This dose of butoxamine decreased the renal vasodilator response to intrarenal isoproterenol by 73%, thus demonstrating significant beta-2 receptor blockade. These results indicate the low-frequency renal nerve stimulation (0.5 Hz) increases renin secretion without altering renal hemodynamics or urinary sodium excretion. This neurally mediated renin secretion resulted from activation of beta-1 adrenergic receptors.

Animals↗
PubMed1984

The effect of sympathomimetic agents on gastric acid secretion in rats.

Beta-adrenoceptor agonists have been reported to inhibit gastric acid secretion in vivo but their site and mode of action is uncertain. A study of the effects of such agents on acid secretion in the rat has been made using both an in vivo preparation and an in vitro one where possible effects due to neural, hormonal or cardiovascular actions of beta-agonists are avoided. In conscious rats with Heidenhain pouches, isoprenaline (40 micrograms kg-1h-1) inhibited the response to pentagastrin (20 micrograms kg-1h-1). This inhibition was abolished by propranolol (2 mg kg-1) and butoxamine (8 mg kg-1) and partially reversed by practolol (8 mg kg-1). Propranolol alone (2 mg kg-1) significantly increased the response to pentagastrin in the pouch rats but butoxamine and practolol (both at 8 mg kg-1) and the inactive isomer (+)-propranolol were without effect on the pentagastrin response. In the rat isolated stomach preparation isoprenaline, salbutamol, salmefamol , adrenaline and nor-adrenaline all stimulated acid output over the range 2 X 10(-7) to 10(-5)M. These responses were antagonised by propranolol (2 X 10(-5)M), pindolol and timolol (10(-6)M) but only nor-adrenaline stimulated secretion was inhibited by the selective antagonists practolol, atenolol, butoxamine and ICI 118551. In vitro responses to beta-adrenoceptor agonists were not antagonised by atropine (10(-5)M), metiamide (10(-4)M) or prostaglandin E2 (10(-5)M).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

The importance of choice of agonist in studies designed to predict beta 2 : beta 1 adrenoceptor selectivity of antagonists from pA2 values on guinea-pig trachea and atria.

1. pA2 values have been obtained for propranolol, butoxamine, H35/25 and atenolol on guinea-pig isolated trachea and atria (rate) using noredrenaline (beta 1-selective), isoprenaline (non-selective) and fenoterol (beta 2-selective) as agonists. 2. pA2 values varied with the agonist used on trachea but not on atria and, therefore, trachea : atria selectivity values varied with the agonist used. 3. It is suggested that the best estimate of the selectivity of an antagonist between beta 2- and beta 1-adrenoceptors is obtained by comparing its pA2 value obtained on trachea using a beta 2-selective agonist with that obtained on atria using a beta 1-selective agonist. The reasons for this are discussed. 4. The quantitative values for beta 2 : beta 1 selectivity obtained using the above pA2 values were butoxamine 17.0 H35/25 13.5, propranolol 2.75 and atenolol 0.036, i.e. butoxamine and H35/25 were beta 2-selective, propranolol was non-selective and atenolol was beta 1-selective. 5. The results support the hypotheses that guinea-pig trachea contains a mixture of beta 1- and beta 2-adrenoceptors and that guinea-pig atria contain only beta 1-adrenoceptors.

Adrenergic beta-Agonists↗
PubMed1986

Calcium levels in rat submandibular gland and saliva after sympathetic nerve stimulation in the presence of alpha, beta 1 and beta 2-adrenergic antagonists.

Calcium concentration was reduced by 51 per cent compared with unstimulated contralateral glands after 60-min of electrical stimulation to the sympathetic nerve. When the alpha-adrenergic antagonists, phentolamine or phenoxybenzamine, were given 20 min before stimulation, the decrease in glandular calcium concentration (45-47 per cent) was similar to that after nerve stimulation alone; with the selective beta 2-adrenergic antagonist added to the phentolamine, the percentage decrease was similar to that found after phentolamine and sympathetic nerve stimulation only. When atenolol, a beta 1-adrenergic antagonist, was given with phentolamine, there was no secretion after subsequent nerve stimulation, nor was calcium concentration different from that of unstimulated glands. When propranolol (3 mg/kg, body wt), or atenolol + butoxamine (3 mg/kg, body wt), was given prior to stimulation there was a decrease of 21-22 per cent in gland-calcium concentration. Calcium concentration of nerve-stimulated saliva was nearly 6 m-equiv./l, and twice as high with phentolamine prior to stimulation; for butoxamine together with phentolamine the change was similar to that with phentolamine alone. When beta-adrenergic antagonists were given prior to nerve stimulation, concentration of the saliva was either unchanged (propranolol) from that with nerve stimulation alone or somewhat decreased (atenolol + butoxamine). Thus sympathetic stimulation results in activation of alpha and beta 1-adrenoceptors; calcium secretion is principally regulated by the beta-adrenoceptors, and beta 1-receptors have the principal role.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

The effect of dobutamine infusion on fractional diaphragm thickening and diaphragm blood flow during fatigue.

BACKGROUND: Diaphragm fatigue (DF) has been implicated in respiratory failure in diseases that increase inspiratory resistance loading (IRL) and may complicate weaning of patients from mechanical ventilation. OBJECTIVE: The purpose of this study was to examine the effects of dobutamine administration (10 micro g/kg/min) on DF and to identify the mechanisms by which dobutamine augments diaphragm shortening and diaphragm blood flow (DBF) during fatigue with a rat model. METHODS: The study had an experimental design with 3 groups of Sprague-Dawley rats (n = 38) with 4 experimental periods: period 1, control; period 2, application of IRL; period 3, treatment; and period 4, recovery. DF was produced via IRL. During period 3 treatment, normal saline solution was infused in group I, dobutamine in group II, and dobutamine plus butoxamine hydrochloride in group III. The percent change in fractional diaphragm thickness (FDT) during inspiration reflected diaphragm shortening. DBF and aortic blood flow were determined with fluorescent microspheres. Diaphragm vascular resistance and systemic vascular resistance were calculated on the basis of Poiseuille's equation. RESULTS: Results indicated infusion of dobutamine increased FDT (P =.01) and DBF (P =.009) with respect to fatigue levels. The effects of dobutamine on FDT and DBF were attenuated with infusion of butoxamine hydrochloride (a beta-2 adrenoceptor antagonist) with respect to fatigue. CONCLUSION: Administration of dobutamine at a rate similar to that used clinically increased diaphragm muscle contractility (FDT) and DBF in diaphragms fatigued by IRL. The dobutamine effect on FDT may be the result of restoration of the balance between diaphragm energy consumption and energy delivery to the diaphragm by increasing DBF. Butoxamine hydrochloride attenuated the dobutamine-induced increase in DBF, indicating dobutamine produced vasodilatation via beta-2 adrenoceptors. Thus, the administration of intravenous dobutamine may be a useful adjunct in the treatment of DF.

Animals↗
PubMedDate not supplied

Effects of some catecholamines on the cat cardiovascular system: interactions with adrenoceptor antagonists.

The effects of intravenous infusions of norepinephrine, epinephrine, isoproterenol, N-t-butylnorepinephrine, oxymethyleneisoproterenol, and RO363 on heart rate, mean arterial blood pressure, cardiac output, total peripheral resistance, and stroke volume were evaluated in chloralose-anaesthetized cats before and after phentolamine, propranolol, atenolol, and butoxamine. Pressor responses to both norepinephrine and epinephrine largely resulted from alpha-receptor-mediated increases in total peripheral resistance. Vasomotor reversal was noted with both drugs in the presence of alpha-receptor blockade. Dilator responses to norepinephrine were abolished by the beta 1-receptor selective antagonist atenolol, as were those to the beta 1-receptor selective agonists oxymethyleneisoproterenol and RO363. Dilator responses to epinephrine were abolished by the beta 2-receptor selective antagonist butoxamine, as were those to N-t-butylnorepinephrine (beta 2-selective) and isoproterenol (nonselective). These results indicate that in addition to beta 2-receptors, beta 1-receptors subserving vasodilatation occur in the cat vasculature. Atenolol displayed agonist-dependent inhibition of the cardiac responses. Responses to noradrenaline, RO363, and oxymethyleneisoproterenol were blocked to a greater extent than were those to epinephrine, N-t-butylnorepinephrine, and isoproterenol. Butoxamine did not display any marked agonist-dependent inhibition of cardiac responses. Nevertheless, the results are in accord with previous suggestions that cardiostimulant beta 2-receptors exist in the cat heart. Interpretation of the actions of catecholamines may be complicated by mixed beta-adrenoceptor populations in the cat cardiovascular system.

Adrenergic beta-Antagonists↗
PubMed1970

The effect of "selective" beta-adrenoceptor blocking drugs on the myocardial circulation.

1. A comparison has been made of the effects of a relatively specific beta(1)-adrenoceptor blocking drug (practolol) and a relatively specific beta(2)-adrenoceptor blocking drug (butoxamine) on myocardial and general haemodynamics in anaesthetized cats.2. Practolol, in a dose (10 mg/kg, intravenously) which had little effect on arterial pressure, heart rate, myocardial blood flow or myocardial vascular resistance, markedly reduced the effects of isoprenaline infusions on heart rate, aortic dp/dt, myocardial blood flow, vascular resistance and metabolic heat production, and the cardiac effort index. Isoprenaline induced vasodepression was unaffected.3. Butoxamine (5 mg/kg, intravenously) decreased heart rate, aortic dp/dt, the cardiac effort index and myocardial blood flow and increased myocardial vascular resistance. This is taken as further evidence for the existence of beta(2)-adrenoceptors in the myocardial microcirculation.4. After butoxamine, the effects of isoprenaline on myocardial blood flow, myocardial vascular resistance and heart rate were unaffected but the peripheral vasodilator effect was abolished. The effects on aortic dp/dt and the cardiac effort index were potentiated.5. It is concluded that the effect of isoprenaline in increasing myocardial blood flow is due predominantly to increased cardiac work and oxygen consumption and that practolol, since it has little direct effect on myocardial blood flow yet abolishes the cardiac stimulant and oxygen wasting effects of released catecholamines, has properties which indicate that it should be an effective and safe anti-anginal drug.

Acetanilides↗
PubMed1981

A comparison of the effects of sympathomimetic agents on gastric acid secretion by the rat stomach in vivo and in vitro.

1. The action of isoprenaline on gastric acid secretion in rats with Heidenhain pouches has been compared with its action in a rat isolated stomach preparation. 2. Isoprenaline (40 micrograms kg-1 h-1) inhibited the acid secretion in response to pentagastrin (20 micrograms kg-1 h-1) in conscious rate with Heidenhain pouches. 3. This inhibition could be abolished by propranolol (2 mg kg-1) and butoxamine (8 mg kg-1) and partially reversed by practolol (8 mg kg-1). 4. Propranolol (2 mg kg-1) significantly increased the response to pentagastrin (20 micrograms kt-1 h-1) but butoxamine and practolol (both at 8 mg kg-1) and the inactive isomer (+)-propranolol (2 mg kg-1) were without any effect on the pentagastrin response in the rats with pouches. 5. In the rat isolated stomach preparation isoprenaline stimulated acid secretion over the range 10(-7) M-10(-3) M whereas phenylephrine and methoxamine were without effect. 6. Propranolol (2 X 10(-5) M) inhibited this stimulatory effect of isoprenaline in vitro but (+)-propranolol (2 X 10(-5) M), practolol and butoxamine (both at 10(-4) M) had no effect on the response. 7. Propranolol (2 X 10(-5) M) did not have any effect on the response of the isolated stomach to pentagastrin (5 X 10(-7) M) or bethanechol (1.7 X 10(-5) M). 8. Phenylephrine (2 X 10(-5) M) did not affect the in vitro responses to pentagastrin (2.17 X 10(-7) M), bethanechol (1.7 X 10(-5) M) or histamine (5.4 X 10(-5) M). 9. It is concluded that isoprenaline has a direct stimulatory effect and an indirect inhibitory effect on gastric acid secretion in the rat. Both effects involve stimulation of beta-adrenoceptors. The relative predominance of one or other of these two opposing effects may help to explain the contradictory results in the literature regarding the actions of beta-adrenoceptor agonists on gastric acid secretion.

Adrenergic alpha-Agonists↗
PubMed1967

A receptor mechanism for the inhibition of insulin release by epinephrine in man.

Normal adult men and women have been infused with epinephrine, 6 mug per minute, during lipolytic blockade with nicotinic acid, beta-adrenergic blockade with propranolol and Butoxamine, and alpha-adrenergic blockade with phentolamine. Epinephrine infusion was associated with low serum levels of immunoreactive insulin (IRI) except when phentolamine was given simultaneously. These findings are compatible with an alpha receptor mechanism for the epinephrine inhibition of insulin release. Phentolamine had no blocking effects on the tachycardia and widened pulse pressure or lipolytic stimulation by epinephrine, whereas both propranolol and Butoxamine blocked lipolysis, tachycardia, and widened pulse pressure. These findings are consistent with an alpha receptor blocking action for phentolamine and beta receptor blocking action for propranolol and Butoxamine. Inhibition of lipolysis by nicotinic acid did not alter IRI or glucose responses to epinephrine. It is concluded that the lipolytic effect of epinephrine is unrelated to its effects on IRI release. Lipolytic blockade by nicotinic acid also did not change IRI or glucose in fasting subjects or their responses to a glucose infusion, 300 mg per minute. These observations appear to conflict with the Randle hypothesis (the glucose-fatty acid cycle) and raise some doubt as to whether plasma FFA concentrations are direct determinants of glucose or IRI concentrations in normal man.

Blood Glucose↗
PubMed1997

The beta2- and beta3-adrenoceptor-mediated relaxation induced by isoprenaline and salbutamol in guinea pig taenia caecum.

To understand the receptor subtypes responsible for beta-adrenoceptor-mediated relaxation of guinea pig taenia caecum, we investigated the effects of isoprenaline and salbutamol. Isoprenaline and salbutamol caused dose-dependent relaxation of the guinea pig taenia caecum. Propranolol, bupranolol and butoxamine produced shifts of the concentration response curves for isoprenaline and salbutamol. Schild regression analyses carried out for propranolol against isoprenaline and salbutamol gave pA2 values of 8.43 and 8.88, respectively. Schild regression analyses carried out for butoxamine against isoprenaline and salbutamol gave pA2 values of 6.46 and 6.68, respectively. Schild regression analyses carried out for bupranolol against isoprenaline and salbutamol gave pA2 values of 8.60 and 8.69, respectively. However, in the presence of 3 x 10(-4) M atenolol, 10(-4) M butoxamine and 10(-6) M phentolamine to block the beta1-, beta2- and alpha-adrenoceptor effects, respectively, Schild regression analyses carried out for bupranolol against isoprenaline and salbutamol gave pA2 values of 5.77 and 5.97, respectively. These results suggest that the relaxant responses to isoprenaline and salbutamol in the guinea pig taenia caecum are mediated by both the beta2- and the beta3-adrenoceptors.

Adrenergic beta-2 Receptor Agonists↗
PubMed1980

Stimulation by beta 2-adrenergic receptors of the production of cyclic AMP and progesterone in rat ovarian tissue.

Ovarian tissue from immature rats treated with pregnant mare serum gonadotrophin (PMSG) or PMSG and human chorionic gonadotrophin was incubated in Medium 199. Stimulation of the formation of cyclic AMP in follicular and luteal tissue by terbutaline (10(-5) mol/l), a selective beta 2-agonist, was blocked by butoxamine (10(-5) mol/l), a selective beta 2-antagonist, whereas practolol (10(-5) mol/l), a selective beta 1-antagonist, was ineffective. Propranolol (10(-5) mol/l) a non-selective beta-antagonist, butoxamine nor practolol affected the increase in cyclic AMP promoted by the addition of 1 microgram LH. Stimulation of the production of progesterone in both follicular and luteal tissue by terbutaline was blocked by butoxamine, but not by practolol. These findings indicated that beta-adrenergic stimulation of ovarian cyclic AMP and progesterone is mediated by beta 2-adrenergic receptors.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

The role of adrenergic mechanism in tremorine-induced tremors in rats: antitremor effect of beta-adrenoceptor antagonists.

Tranylcypromine (TCP) pretreatment was found to accelerate the tremorogenic activity of tremorine in rats. Conversely, reserpinization delayed the onset of induction of tremors, and a significant diminution in their intensity was observed in these rats. A comparative study of the antitremor activity of beta-adrenoceptor antagonists against this tremor-model showed that butoxamine (beta 2-antagonist) and propranolol (nonselective antagonist) were able to afford a rapid and powerful protection, whereas a weaker and delayed effect was observed in rats treated with the beta 1-antagonist, acebutolol. Furthermore, the antitremor activity of butoxamine and propranolol but not that of acebutolol was found to be potentiated and diminished in rats pretreated with reserpine and TCP, respectively. It was inferred that beta 2-receptor modulated the tremorogenic activity of tremorine, and that inhibition by propranolol or butoxamine of this subtype beta-adrenoceptor resulted in rapid and powerful suppression of tremors, and that the antiadrenergic activity of acebutolol was unlikely to have a role in its antitremor effect.

Adrenergic beta-Antagonists↗