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PubMed1976

The pharmacokinetic characteristics of beta-receptor antagonists in man--similarities and differences of clinical relevance.

The aliphatic partial structure common to the beta-receptor antagonists leads to similar products of their biotransformation. The main qualitative and quantitative differences of the metabolism of the compounds of this class, however, rest in the nature of their aromatic or heterocyclic substituents. The physico-chemical properties of the beta-blockers appear to be predominantly responsible for the extent of metabolic degradation and for the distribution in the body, especially for the binding to proteins. As a consequence of their different biological disposition the clinically relevant systemic bioavailabilities of the various beta-blockers from oral doses differ drastically. Practolol maintains an extreme position among all other compounds: It is most hydrophilic, it is not bound to proteins, it is metabolized least, but cleared renally in unchanged form to 85% of the dose. Despite its extremely high systemic bioavailability, relatively high daily doses were required for therapy. The receptor sensitivity for practolol has been rated 2 to 3 powers of 1- lower than of propranolol. Comparative pharmacokinetic assessment of beta-receptor antagonists requires quantitative analytical data in clinically representative groups of patients. This has been demonstrated by respective studies with oxprenolol. The intra- and inter-individual systemic bioavailability, the differential analysis of plasma and erythrocytes, the multiexponential elimination kinetics, and their possible dependence on the dose have been studied as clinically relevant pharmacokinetic characteristics. The continuing attempt of the pharmaceutical industry to optimize the properties of beta-blockers also has taken advantage of the slow release principle in oral dosage forms as shown by the example of oxprenolol. The beta-receptor antagonists belong to one of the youngest classes of pharmaceuticals. Pharmacokinetic and metabolic data for the different representatives of this class have been generated in different laboratories with different approaches and different techniques. Therefore, full comparative documentation is still incomplete.

Adrenergic beta-Antagonists↗
PubMed1970

Comparative chronotropic activity of beta-adrenoceptive antagonists.

1. Chronotropic dose-response curves (non-cumulative) for beta-adrenoceptive antagonists were constructed from results in rats anaesthetized with pentobarbitone and depleted of catecholamines by pre-treatment with syrosingopine.2. Depletion of catecholamines lowered resting heart rate and reduced the threshold to the chronotropic action of isoprenaline by about 50%. Eight beta-adrenoceptive antagonists produced a dose-dependent chronotropic response but the maximum response was in all cases smaller than that obtained with isoprenaline. The order of activity was dichloroisoprenaline>LB 46>practolol>INPEA>oxprenolol>pronethalol>alprenolol>I.C.I. 45,763 (Kö 592). Propranolol and sotalol were without significant activity. The duration of the chronotropic response to the antagonists was more prolonged than that to isoprenaline. Propranolol caused a parallel shift to the right of the dose-response curves for the agonist effects of the antagonists.3. Estimation of beta-adrenoceptor blocking activity in anaesthetized cats gave an order of activity dissimilar to that found for maximum agonist responses: LB 46 > oxprenolol > alprenolol > propranolol > I.C.I. 45,763 > practolol > dichloroisoprenaline > sotalol > INPEA > pronethalol.4. Consideration of chemical structure and physico-chemical properties did not explain the differences between the agonist activities of the adrenoceptive antagonists.

Acetanilides↗
PubMed1972

Characterization of the coronary vascular -adrenoceptor in the pig.

The beta-adrenoceptor in pig coronary vascular smooth muscle has been characterized by the use of a selective agonist, salbutamol and a selective antagonist, practolol. In coronary artery strips contracted with KCI, salbutamol had only marginal relaxant activity and was a partial agonist compared with isoprenaline. Practolol had relatively high antagonist potency against isoprenaline (pA(2) 6.59). It is concluded that the pig coronary vascular,beta-adrenoceptor is of the beta(1)-type.

Acetanilides↗
PubMed1972

Effect of -adrenoceptor blocking agents on poststimulatory atrial flutter in the dog, with observations on the participation of adrenergic mechanisms in this experimental arrhythmia.

1. Four beta-adrenoceptor antagonists, viz. (+/-) propranolol (0.5 mg/kg), (-) alprenolol (0.25 mg/kg), practolol (5 mg/kg) and USVC 6524 (20 mug/kg), were tested for their effects on atrial flutter produced by electrical stimulation of the right atrium around the crushed inter-venae-caval bridge in anaesthetized dogs.2. All the drugs reduced atrial and ventricular rates; this was followed by the abrupt termination of flutter and restoration to normal sinus rhythm.3. Since all the drugs (including practolol, which is devoid of local anaesthetic activity) were given in doses just sufficient to block beta-adrenoceptors, it indicated that beta-adrenoceptor blockade was responsible for their antiarrhythmic property in this test procedure.4. Further evidences in support of participation of the sympathetic nervous system in poststimulatory flutter were: (i) flutter could not be produced in nine out of ten dogs whose catecholamine stores were depleted by pretreatment with reserpine; (ii) infusion of adrenaline in these animals resulted in the production of flutter; (iii) duration of flutter after termination of exposure to adrenaline was a few minutes, which is similar to the brief time previously reported to be taken for the disappearance of catecholamines from the hearts of reserpinized animals.5. The clinical significance of the above findings is discussed.

Acetanilides↗
PubMed1972

Assessment of the effectiveness of -adrenoceptor blocking agents towards cardiac and bronchiolar responses of the pithed guinea-pig to electrical stimulation of the spinal outflow.

1. The responses of heart rate and resistance to lung inflation of the pithed guinea-pig on electrical stimulation of the thoracic spinal roots could be related to similar responses to injected catecholamines, such that dose-stimulus frequency relations could be plotted.2. The range of frequency of stimulation that was equi-effective with a dose range of injected catecholamines was higher for effects on air overflow than for heart rate. The slope of the relations for heart rate also differed from that for air overflow. These features may reflect a difference in effectiveness of the sympathetic innervation of heart and bronchial tree.3. Propranolol was equally effective in reducing the responses of heart rate and air overflow to injected noradrenaline. Practolol was somewhat more active against the effects of noradrenaline on air overflow than on heart rate, though equally active against the effects of isoprenaline.4. For the assessment of equivalent blockade of the effects of cord stimulation on heart rate and air overflow, frequency-ratios corresponding to a noradrenaline dose-ratio of 2 were derived from the slopes of the dose-frequency relations; for air overflow this value was approximately 2 and for heart rate approximately 1.4.5. When the doses required to produce these degrees of blockade were computed from the dose-response relations for blockade of the effects of cord stimulation by propranolol, they were found to be similar for effects on heart rate and air overflow. For practolol, the effective dose for block of heart rate increase was found to be lower than that for air overflow.

Acetanilides↗
PubMed1976

Selectivity of beta-adrenoceptor agonists and antagonists on bronchial, skeletal, vascular and cardiac muscle in the anaesthetized cat.

1 The potencies of fifteen beta-adrenoceptor agonists of widely differing chemical structures were compared with that of (-)-isoprenaline on bronchial muscle, soleus muscle, blood pressure and heart rate in the anaesthetized cat. The beta-adrenoceptor antagonist potencies of propranolol and practolol were determined against (-)-isoprenaline in the same model. 2 (-)-Isoprenaline was the most potent agonist and its action was essentially unselective. Thus, on all four parameters the minimal effective dose was 0.003-0.01 mug/kg and maximal or near maximal responses were produced by 0.3-1 mug/kg. Trimetoquinol was also an essentially unselective agonist. 3 For thirteen of the remaining fourteen agonists, potency was similar on bronchial muscle, soleus muscle and blood pressure but significantly lower on heart rate. 4 The remaining agonist - AH 7616 (4-hydroxy-alpha1-[[(1-methyl-3,3-diphenyl-propyl)amino]-methyl]-m-xylene-alpha1, alpha3-diol, acetate) - was also significantly less potent on heart rate than on the other parameters; in addition, it was clearly less potent on soleus muscle and blood pressure than on bronchial muscle when 5-hydroxytryptamine (5-HT) was used to induce bronchospasm. However, when acetylcholine was used instead of 5-HT the potency of AH 7616 on induce bronchospasm. However, when acetylcholine was used instead of 5-HT the potency of AH 7616 on bronchial muscle, soleus muscle and blood pressure was very similar. AH 7616 may therefore possess a specific 5-HT antagonist action in addition to its beta-adrenoceptor agonist action. 5 The fifteen test agonists were longer acting than (-)-isoprenaline and this was particularly true of trimetoquinol and soterenol. 6 The beta-adrenoceptor antagonist potency of propranolol was almost identical on bronchial muscle, soleus muscle and blood pressure and very slightly lower on the heart. Practolol was 10-12 times more potent on the heart than on bronchial muscle, soleus muscle and blood pressure. 7 These findings suggest that it may not be possible to separate the bronchodilating and tremorenhancing properties of beta-adrenoceptor agonists. The results with agonists and antagonists are in accord with Lands' dual beta-adrenoceptor sub-classification.

Adrenergic beta-Agonists↗
PubMed1978

Evidence for the participation of beta1-adrenoceptors in isoprenaline-induced renin release from rat kidny slices in vitro.

1. The inhibitory effects were studied of 4 beta-adrenoceptor antagonists against renin release induced by isoprenaline (0.5 mumol/1) in rat kidney slices. Additionally the pA2 values of these 4 drugs were measured against isoprenaline in guinea-pig isolated atria and trachea (against beta1- and beta2-adrenoceptors respectively). 2 When employed at a concentration of 2 mumol/1 propranolol and atenolol significantly inhibited renin release (P less than 0.001 and P less than 0.01) whereas practolol and IPS 339 [t-butyl-amino-3 ol-2 propyl) oximino-9 fluorene] had little effect. 2 A positive correlation was shown between the degree of inhibition of renin release and the pA2 of the antagonists at the beta1-adrenoceptors. 4 When practolol and IPS 339 were used in equipotent molar concentrations to propranolol for the beta1-adrenoceptors they inhibited renin release. 5 The results suggest that the adrenoceptor involved in the renin release induced by isoprenaline in the rat kidney is of the beta1-type.

Adrenergic beta-Antagonists↗
PubMed1980

Influence of beta-adrenoceptor blocking agents on the turnover rate of cardiac and splenic noradrenaline in rats.

1 The effects of (+) and (+/-)-propranolol, pindolol, alprenolol, practolol, acebutolol and bretylium were studied on the turnover rate of noradrenaline in heart and spleen of rats. 2 Bretylium (8 mg/kg) greatly reduced the turnover rate of noradrenaline in both organs. 3 (+)-Propranolol (4 and 10 mg/kg) also diminished the turnover rate of noradrenaline, but its effects were smaller than those of (+/-)-propranolol (4 and 10 mg/kg). 4 Pindolol (300 micrograms/kg) greatly increased the turnover rate of noradrenaline; this effect was especially important in the spleen. 5 Alprenolol (4 and 10 mg/kg) acebutolol (20 and 40 mg/kg) practolol (10 mg/kg) did not produce any significant change. 6 These effects are compatible with the view that beta-adrenoceptor blocking agents may affect noradrenaline release in different manners: anaesthetic properties of some of these drugs and blockade of beta 2 prejunctional adrenoceptors produce a diminished release of transmitter, whereas the intrinsic sympathomimetic action of pindolol causes the opposite effect.

Adrenergic beta-Antagonists↗
PubMed1982

Role of central beta-adrenoceptors in the control of pentylenetetrazol-induced convulsions in rats.

1 The role of central beta-adrenoceptors in the anticonvulsant effect of beta-adrenoceptor antagonists has been examined. 2 Oral administration of (-)- and (+)-propranolol (0.05-1 mg/kg) and (+/-)-pindolol (0.025-0.5 mg/kg) produced a dose-dependent decrease in duration of convulsions produced by pentylenetetrazol (PTZ 50 mg/kg, i.p.) in rats. 3 At the EC50 level, (-)-propranolol is seven times more effective than the (+)-isomer. 4 Oral administration of (-)-, (+)- or (+/-)-practolol (1-10 mg/kg) or (-)- or (+)-timolol (1-10 mg/kg), two beta-adrenoceptor antagonists that do not penetrate the blood brain barrier, had no significant effect on the duration of PTZ-induced convulsions. 5 Intracerebroventricular administration of (-)-propranolol (0.5 microgram/kg) or (-)-timolol (0.25 microgram/kg) produced highly significant anticonvulsant effects whereas the (+)-isomers at the same dose level were ineffective. (+/-)-Pindolol (0.25 microgram/kg) was also much more effective given by this route than when given orally. The (+)- and (-)-isomers of the beta 1-adrenoceptor selective antagonist practolol (10 microgram/kg) exerted only weak anticonvulsant effects. 6 This study provides evidence that beta-adrenoceptor antagonists exert an anticonvulsant effect through central beta 2-adrenoceptors. At high dose levels, additional anticonvulsant activity is associated with membrane stabilization in those antagonists which possess this property.

Adrenergic beta-Antagonists↗
PubMed1983

The effect of beta-adrenoceptor blocking agents, with differing ancillary properties, on the arrhythmias resulting from acute coronary artery ligation in anaesthetized rats.

The effects of several beta-adrenoceptor blocking agents, [+), (-) and (+/-)-oxprenolol, p-oxprenolol, practolol, propranolol and timolol) were investigated on the ventricular arrhythmias occurring within the first 30 min of acutely ligating the main left coronary artery in anaesthetized rats. The degree of cardiac and vascular beta-adrenoceptor blockade was also assessed. All the compounds exhibited antiarrhythmic activity under these conditions. The degree of cardiac beta-adrenoceptor blockade required for this protection was less for the cardioselective agents, p-oxprenolol and practolol, than for the non-selective beta-adrenoceptor blocking agents. A comparison of the two isomers of oxprenolol demonstrated that the (-)-isomer markedly suppressed ischaemic arrhythmias (ventricular ectopic beats, incidence and duration of ventricular tachycardia and duration of ventricular fibrillation) more effectively than the (+)-isomer. Compounds possessing intrinsic sympathomimetic activity (ISA) caused less marked haemodynamic changes (in equivalent beta-blocking doses) than those that did not possess this ancillary property. The membrane stabilizing activity of oxprenolol and p-oxprenolol did not appear to contribute to the antiarrhythmic activity of these agents; however, the membrane stabilizing activity of propranolol may contribute to its effectiveness. In all the drugs studied, the main pharmacological property required to suppress early postischaemic arrhythmias is blockade of cardiac beta-adrenoceptors.

Adrenergic beta-Antagonists↗
PubMed1983

Depolarization of rat isolated superior cervical ganglia mediated by beta 2-adrenoceptors.

Depolarizations of freshly-dissected isolated superior cervical ganglia of the rat were recorded extracellularly. The following sympathomimetic amines (in order of decreasing potency) produced depolarizations of up to 0.4 mV: isoprenaline, salbutamol, adrenaline, noradrenaline. Depolarizations were lost after overnight storage, leaving only hyperpolarizing responses. Depolarizations by isoprenaline were antagonized by (-)-propranolol (pA2 8.94 +/- 0.15), (+/-)-butoxamine (pA2 7.36 +/- 0.12) and (+/-)-practolol (pA2 5.14 +/- 0.13). They were not blocked by phentolamine (1 microM) or phenoxybenzamine (1 microM). Isoprenaline and salbutamol were antagonized with equal facility by practolol or butoxamine. In concentrations producing ganglionic depolarization, these compounds also produced a smaller depolarization of presynaptic elements in the ganglion, but not preganglionic trunk fibres. Presynaptic depolarization was blocked by 100 nM propranolol but not by 1 microM phentolamine. Isoprenaline and salbutamol increased the amplitude of the compound ganglionic action potential recorded following single preganglionic nerve stimuli when transmission had been rendered submaximal by adjusting the Ca/Mg ratio, but not in normal solution. Isoprenaline (0.1 microM) also increased the amount of [3H]-acetylcholine released by preganglionic stimulation in low Ca/high Mg solution. It is concluded that facilitatory adrenoceptors are present on pre- and postsynaptic elements in rat superior cervical ganglia, which resembles the 'beta 2' subclass of beta-receptors.

Acetylcholine↗
PubMed1986

The antinociceptive action of some beta-adrenoceptor agonists in mice.

The antinociceptive actions of several beta-adrenoceptor agonist drugs have been studied in mice by use of a modified abdominal constriction test. All the drugs studied had high antinociceptive activity, with ID50 values in the nmol kg-1 range. (-)-Isoprenaline and (+/-)-isoxsuprine were the most potent, being about ten times more active than salbutamol, the least potent drug studied. All these drugs produced their action very rapidly and appear to act within the peritoneum. (-)-Isoprenaline had about six times the potency of the (+)-isomer. (+/-)-Propranolol caused rightward shifts, usually parallel, of the dose-response curves for (-)-isoprenaline. (+)-Propranolol was more than ten times less potent than the racemic drug. Practolol also caused parallel, rightward shifts of the dose-response curves for (-)-isoprenaline, and was about twice as potent as (+/-)-propranolol, whether given by subcutaneous or intraperitoneal injection. Atenolol and ICI 118551 had intermediate potencies. Propranolol, practolol and ICI 118551 were all considerably less potent in antagonizing the antinociceptive actions of fenoterol and RO363, than (-)-isoprenaline. None of these antagonist drugs showed more than a slight ability to discriminate between the beta 1- and beta 2-selective agonist drugs. No evidence was found for the involvement of opioid, dopamine, or alpha-adrenoceptors in the antinociceptive action of the beta-adrenoceptor agonist drugs. Evidence for and against the involvement of beta-adrenoceptors is discussed, and it is concluded that if these receptors do mediate the antinociceptive action they appear to be atypical.

Adrenergic beta-Agonists↗
PubMed1986

Investigation into the cardioregulatory properties of the alpha 1-adrenoceptor blocker indoramin.

The cardioregulatory properties of the alpha 1-adrenoceptor blocker indoramin have been compared with those of prazosin in the anaesthetized rat. The effects of autonomic blockade on heart rate responses evoked by these two agents and their effects on blood pressure and heart rate after peripheral or central administration have been compared. Cumulative administration of indoramin (0.8-25.6 mg kg-1 i.v.) evoked significant decreases in arterial blood pressure and a concomitant bradycardia. Pithing or autonomic blockade, by pretreatment with a combination of practolol and bilateral vagotomy, prevented the bradycardia evoked by indoramin (0.8-3.2 mg kg-1 i.v.). Atropine sulphate pretreatment abolished the bradycardia until a cumulative dose of 25.6 mg kg-1(i.v.) of indoramin had been reached. Bilateral vagotomy, intravenous administration of atropine methylnitrate or practolol pretreatment attenuated the bradycardia. Prazosin (0.02-0.64 mg kg-1 i.v.) evoked a fall in arterial blood pressure of similar magnitude to that observed following indoramin. A bradycardia was evoked only at a relatively high dose (0.64 mg kg-1 i.v.). Intracisternal injection of indoramin or prazosin evoked bradycardia and hypotension at a dose which had no effect after intravenous injection (25 micrograms). Intracerebroventricular injection of indoramin (25 micrograms) had no significant effect on heart rate or blood pressure compared to control values, whereas prazosin (25 micrograms) evoked a significant tachycardia and hypotension. It is concluded that the bradycardia evoked by indoramin in the rat is not due to a direct action on the heart except possibly at high doses. Central alpha 1-adrenoceptor blockade, possibly in the brainstem region, results in a bradycardia and this may explain the lack of reflex tachycardia following the administration of indoramin.

Animals↗
PubMed1991

Different mechanisms of action of agents acting on beta-adrenoceptors in barium-stimulated and electrically-stimulated rat vas deferens.

1. The relaxation induced by beta-adrenoceptor agonists in rat vas deferens was examined under two different experimental conditions: on electrically-induced twitch responses (35 V, 3 ms, 0.07 Hz), and on contractions induced by single doses of barium chloride (300 microM). The experiments were performed in vasa of reserpine-treated rats, after blockade of alpha-adrenoceptors and extraneuronal uptake with dibenamine (10 microM, 30 min), and neuronal uptake with cocaine (10 microM). 2. When twitch responses were used, the values of pD2, interpolated from cumulative concentration-response curves for isoprenaline (Iso), adrenaline (Ad), and noradrenaline (NA) showed a rank order of potency consistent with the presence of beta 2-adrenoceptors (Iso greater than Ad much greater than NA). 3. When twitch responses were used, the non-selective beta-antagonist, propranolol, caused a concentration-dependent parallel shift to the right of Iso concentration-response curves. Similar shifts were obtained by use of the beta 2-antagonist, isopropylmethoxamine (IMA), and higher doses of the beta 1-antagonist, practolol, according to the expectations from receptor occupation theory. Practolol presented the lowest value of pKB, 5.03, corroborating the presence of beta 2-adrenoceptors. 4. When twitch responses were used, and Ad or NA employed instead of Iso, the antagonists produced shifts of concentration-response curves which were smaller than expected from theory, precluding the determination of pKB values. This indicates that other mechanisms are involved besides an interaction with a single population of postsynaptic beta 2-adrenoceptors. 5. When barium chloride was used instead of twitch responses, although the potencies of Iso and Ad were increased respectively by about 30 fold and 5 fold, the rank order of potency was still consistent with an interaction with beta 2-adrenoceptors. In addition, the antagonists produced parallel and concentrationdependent shifts of the curves of all the agonists, as expected from receptor theory. The values of pKB for a given antagonist were not modified by interchanging the agonists used, indicating a typical interaction with a single population of beta 2-adrenoceptors. When compared to the field-stimulated vas, the values of pKB for propranolol and IMA against isoprenaline were respectively 1.3 and 0.6 log units larger. These results suggest the beta l-adrenoceptor agents act by different mechanisms of action in barium-stimulated and electrically-stimulated vas. 6. It is suggested that when barium is used, the effects of agents acting on beta l-adrenoceptors are mediated only by postsynaptic beta 2-receptors, while other complicating factors, probably nerve-dependent presynaptic mechanisms, may be involved with electrical stimulation.

Adrenergic beta-Agonists↗
PubMed1996

Effects of beta-adrenoceptor antagonists on Ca(2+)-overload induced by lysophosphatidylcholine in rat isolated cardiomyocytes.

1. The effects of beta-adrenoceptor antagonists including (-)- and (+)-propranolol, (-)- and (+)-penbutolol, timolol, pindolol, atenolol, acebutolol and practolol on the Ca(2+)-overload induced by lysophosphatidylcholine (LPC) were examined in isolated cardiomyocytes of the rat. 2. Fura-2 was used for measurement of the intracellular calcium concentration ([Ca2+]i). LPC (15 microM) produced a rapid increase in [Ca2+]i from 72 +/- 5 to 3042 +/- 431 nM which coincided with a decrease in the percentage of rod-shaped cells from 69 +/- 2 to 5 +/- 2%. 3. Preincubation with (-)-propranolol (20 microM), (+)-propranolol (50 microM), or (-)- or (+)-penbutolol (20 microM), the lipophilicity of which is higher than other beta-adrenoceptor antagonists, significantly inhibited both the increase in [Ca2+]i and the cell-shape change induced by 15 microM LPC. The inhibitory effects of the four drugs on the LPC-induced increase in [Ca2+]i and cell-shape change were concentration-dependent. The IC50S of (-)-propranolol, (+)-propranolol, (-)- and (+)-penbutolol for the increase in [Ca2+]i were 1.28, 10.50, 0.67 and 0.76 microM, respectively. 4. Pretreatment with pindolol, timolol, acebutolol, practolol, atenolol or lignocaine did not inhibit the increase in [Ca2+]i and the morphological change induced by LPC. 5. LPC markedly increased the release of creatine phosphokinase from 9 +/- 1 to 45 +/- 2% which could be significantly reduced by (-)- or (+)-propranolol but not by acebutolol or timolol. 6. The protective effects of (-)- and (+)-propranolol, (-)- and (+)-penbutolol against the Ca(2+)-overload induced by LPC were not associated with the beta-adrenoceptor antagonistic action, but probably with an unknown action which is related to the preservation of membrane integrity. Further studies are necessary to clarify the exact mechanisms of the protective action of these beta-adrenoceptor antagonists against the Ca(2+)-overload induced by LPC.

Adrenergic beta-Antagonists↗
PubMed1989

Conjunctival keratinisation, an abnormal reaction to an ocular beta-blocker.

Conjunctival leucoplakia was induced by the local beta-blocker metipranolol in one case. Withdrawal of the drug and application of all-trans retinoic acid ointment resulted in resolving of the keratinisation. A striking pharmacological resemblance is discovered between metipranolol and practolol. Metipranolol seems to be a less toxic phenol derivative of practolol. Nevertheless, it seems able to act as antigen.

Chemical Phenomena↗
PubMed1983

Beta 2-adrenoceptors in guinea-pig atria.

The occurrence of beta 2-adrenoceptors in the isolated, spontaneously beating right atrium and the electrically driven left atrium of the guinea-pig was studied. Isoprenaline was used as reference compound and procaterol as selective beta 2-agonist. Cumulative concentration response (C/R) curves were obtained with the agonists. The C/R curve of procaterol was biphasic in both preparations. Compared with isoprenaline, procaterol was a partial agonist, with a mean maximum response of 0.78 +/- 0.04 in the right atrium and 0.29 +/- 0.05 in the left atrium. The beta 2-selective antagonist ICI 118,551, 10(-7) mol litre-1, caused a small but significant shift of the C/R curve of isoprenaline to a higher concentration range in both preparations. The same concentration of the beta 2-blocker changed the shape of the C/R curve of procaterol from biphasic to monophasic by blocking the responses to low concentrations of procaterol. Practolol, a beta 1-selective antagonist, 10(-6) mol litre-1, gave a highly significant shift of the C/R curve of isoprenaline to a higher concentration range in both preparations but had no effect on the responses to low concentrations of procaterol. The effect of practolol on the responses to high concentrations of procaterol is discussed. We conclude that the guinea-pig atria may contain beta 2-adrenoceptors mediating positive chronotropic and inotropic effects.

Animals↗
PubMed1985

Identification of adrenoceptors and dopamine receptors mediating vascular responses in the superior mesenteric arterial bed of the rat.

The nature of the adrenoceptors and dopamine receptors mediating vascular responses in the in-situ blood perfused superior mesenteric arterial bed of the rat have been studied. alpha 1-Adrenoceptor agonists produced vasoconstriction but alpha 2-agonists had no significant effect on vascular resistance. The vasoconstrictor effects of noradrenaline were antagonized by low doses of prazosin (26 nmol kg-1 i.v.). Isoprenaline and salbutamol produced vasodilation when the vasculature was preconstricted with arginine vasopressin. The responses to isoprenaline were potently antagonized by propranolol (1.69 mumol kg-1 i.v.) and weakly but significantly reduced by practolol (3.75 mumol kg-1 i.v.) whereas the responses to salbutamol were unaffected by the same dose of practolol. After preconstriction of the vasculature and alpha-adrenoceptor blockade, dopamine and apomorphine produced dilator responses with both compounds producing the same maximal response and apomorphine being 1.8 times more potent than dopamine. The dopamine responses were present after the animals had been pithed and were resistant to spiperone (506 nmol kg-1 i.v.) but were antagonized by cis-alpha-flupenthixol (460 nmol kg-1 i.v.). These results suggest that this vascular bed possesses vasoconstrictor alpha 1- but not alpha 2-adrenoceptors, vasodilator beta 1- and beta 2-adrenoceptors and vasodilator dopamine receptors which appear similar to the D1-type found centrally.

Animals↗