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At least 739 records · Page 41Linked to original sources
PubMed1981

Characterization of beta-adrenoceptors in the dog saphenous vein.

In vitro experiments were carried out on strips of the dog saphenous vein to characterize beta-adrenoceptors mediating relaxation. Four beta-adrenoceptor agonists, isoproterenol, salbutamol, procaterol and alpha-(3,4,5-trimethoxyphenethylaminomethyl)-3,4-dihydroxybenzylalcohol hydrochloride (T-1583), all produced concentration-dependent relaxation of venous strips contracted by 10(-6) M methoxamine. These four drugs behaved as full agonists. In producing venous relaxation, procaterol was about 2.5 times more potent, and salbutamol and T-1583 were 7 and 98 times less potent than isoproterenol, on a molar basis. The concentration-relaxation response curves to the four agonists were shifted in a parallel way to the right by (t-butyl-amino-3-ol-2-propyl)oximino-9 fluorene hydrochloride (IPS 339), a selective beta 2-adrenoceptor antagonist, and by practolol. However, pA2-values for IPS 339 against the four agonists were all nearly 11.0, whereas those for practolol were all nearly 5.7. We conclude that beta-adrenoceptors in the dog saphenous vein mediating relaxation are predominantly on the beta 2 type.

Adrenergic beta-Agonists↗
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↗
PubMed1975

Effects of terbutaline on human uterine motility at term.

The effects of the selective beta-2-receptor stimulator terbutaline on the activity of gravid, human myometrium were investigated in vitro and in vivo, before and after administration of different beta-receptor blockers. Terbutaline, 0.2-1.0 mu-g/ml, inhibited the spontaneous contractile activity of isolated strips of myometrium. This effect was unaffected by the selective beta-a-receptor blockers practolol, 1 mu-g/ml, and H 93/26, 1 mu-g/ml. However, the non-selective blocker propranolol, 0.1 mu-g/ml, completely inhibited the terbutaline effects. The in vitro effects of terbutaline could be correlated with findings in vivo. Intra-uterine pressure was recorded in 4 pregnant women at term. Infusion of terbutaline, 10-15 mu-g/min, for 20-40 min, effectively inhibited both spontaneous and oxytocin-stimulated uterine activity. There was a moderate increase in maternal heart rate, but no consistent effect on maternal blood pressure. Fetal heart rate was little affected. The uterine effects of terbuline were not influenced by practolol, 5-20 mg i.v., but completely inhibited by propranolol, 1-2 mg i.v. The results suggest that terbutaline inhibits uterine motility by effects on uterine beta-2-receptors and that it can be given in clinically effective doses without adverse circulatory effects on mother or fetus.

Adult↗
PubMed1980

Effect of two types of beta-adrenergic blockade on gastric acid secretion during basal conditions and during histamine stimulation on non-vagotomized and in vagotomized gastric fistula dogs.

The effect of beta-adrenoreceptor blockade by propranolol and practolol on basal secretion and on submaximally histamine-stimulated gastric acid secretion was studied in conscious non-vagotomized and in vagotomized gastric fistula dogs. Neither propranolol (0.5 mg/kg) nor practolol (1.0 mg/kg), both intravenously, had a significant influence on basal or histamine-stimulated gastric acid secretion in non-vagotomized and vagotomized dogs. It is concluded that beta-adrenergic blockade has no influence on basal or histamine-stimulated gastric acid secretion in dogs. Furthermore, no differences were found between the non-vagotomized and the vagotomized stomach.

Adrenergic beta-Antagonists↗
PubMed1980

Disposition in rats and mice of chloropractolol, a new beta-blocking agent.

1. The disposition of a new beta-blocking agent, chloropractolol, labelled with 14C and with 3H, has been studied in rats and mice. 2. After i.v. administration to the rat (25 mg/kg) of a mixture of [14C]- and [3H]chloropractolol, urinary and faecal excretion, biliary elimination and tissue distribution were similar for the two labelled species. However, 3% of the dose was recovered as 14CO2. 3. Chloropractolol and/or metabolites did not show high cardioselectivity. Uptake by heart of the two labelled species was very close to that found for [14C]practolol and [14C]propranolol. 4. Preliminary metabolic studies using h.p.l.c. have shown that in the rat chloropractolol is extensively metabolized, which contrasts with the more limited metabolism of practolol in the same species. Deacetylation is a minor route of metabolism. A structure for the main urinary metabolite is suggested.

Adrenergic beta-Antagonists↗
PubMed1976

Effect of acebutolol, a new beta-receptor antagonist on heart rate and rate-pressure product in normal subjects.

A study on the effect of acebutolol, a new beta receptor antagonist, on the resting and post-exercise heart rate and rate-pressure product was carried out in 8 normal volunteers. Intravenous administration of 10 and 20 mg acebutolol was compared with 10 and 20 mg practolol administered at weekly intervals. In the oral study, increasing doses of acebutolol were administered over a period of 20 days. The heart rate and blood pressure was recorded before and at the completion of 4-minute exercise period. The exercise was carried out on a bicycle ergometer at 150 watt per minute for 4 minutes. In a dose to dose comparison, the potencies of acebutolol and practolol administered intravenously were of the same order, in decreasing the resting and post-exercise heart rate and rate pressure product. Their duration of action was also similar. In the oral study, the peak effect was achieved at a dosage of 200 mg per day (100 mg twice daily) of acebutolol. Acebutolol decreased the resting as well as post-exercise rate-pressure product (cardiac work load). This may be the mechanism for the reported beneficial effect in angina pectoris. Acebutolol was well tolerated and no serious side-effects were observed.

Acebutolol↗
PubMed1977

[Effect of beta-adrenergic blockaders on the uterine musculature of rats].

The authors carried out a study on beta-adrenergic blockers Proprafnolol, Pindolol and Practolol, on an isolated uterus of a rat, obtained at various phases oestrus. The Beta-adrenergic blocker Pindolol manifested inhibiting effect on the spontaneous contractility of the uterus more marked after elevated level of gestagens. The pharmacological analysis gave foundation to the authors to assume that the relaxation of Pindolol was due to direct myotropic action. Propranolol in large doses and at high gestagenic level manifested antioxytocic activity. Practolol did not affect both spontaneous uterine activity as oxytoxin contraction.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Pharmacological responses to dopamine in isolated guinea-pig cardiovascular tissues: mechanisms of action.

The mechanisms responsible for the positive inotropic, positive chronotropic and vasoconstrictor responses to dopamine in isolated guinea-pig cardiovascular tissues have been investigated in the present study. Since dopamine is the immediate precursor of noradrenaline, the role of noradrenaline in the pharmacological responses after addition of dopamine has been assessed. In isolated, contracting right ventricular papillary muscles, dopamine-induced positive inotropy (-log EC50, 4.77 +/- 0.06) was unaltered by incubation with dopamine antagonists (SCH 23390, domperidone), alpha-adrenoceptor antagonists (prazosin, yohimbine), or an inhibitor of uptake1 (cocaine). Practolol (selective beta 1-adrenoceptor antagonist) and ICI 118,551 (selective beta 2-adrenoceptor antagonist) were noncompetitive antagonists to dopamine. Block of vesicular uptake by reserpine antagonized the positive inotropic responses to dopamine (-log EC50, 4.03 +/- 0.05) but not to noradrenaline; these responses were antagonized by both practolol and ICI 118,551. Chemical sympathectomy by 6-hydroxydopamine antagonized the responses to dopamine (-log EC50, 3.76 +/- 0.11) but potentiated the responses to noradrenaline (-log EC50, 7.35 +/- 0.07). Inhibition of monoamine oxidase with pargyline potentiated the responses to dopamine (-log EC50, 6.05 +/- 0.04) and noradrenaline; the potentiation of dopamine responses was unaffected by chemical sympathectomy. Inhibition of dopamine beta-hydroxylase with sodium diethyldithiocarbamate antagonized the inotropic responses to dopamine (-log EC50, 4.36 +/- 0.05) but not to noradrenaline. Similar results were obtained in guinea-pig left atria (positive inotropy) and right atria (positive chronotropy), except that chemical sympathectomy failed to affect the chronotropic responses. In thoracic aortic rings, dopamine contracted vascular smooth muscle by direct partial agonism of alpha 1-adrenoceptors, without involvement of dopamine beta-hydroxylase. Thus, there is antagonism of the cardiac, but not the vascular responses to dopamine by inhibition of dopamine beta-hydroxylase. This shows that the conversion of dopamine to noradrenaline is important in the inotropic and chronotropic responses, but not the vascular responses to dopamine.

Adrenergic beta-Antagonists↗
PubMed1975

[Plasma renin activity and plasma aldosterone during anaesthesia and operative stress and beta-adrenergic blockade (author's transl)].

In 21 patients undergoing ear operations associated with minimal bleeding plasma renin activity and plasma aldosterone concentration were studied before and during surgical procedure, and in the postoperative state. Studies were performed in two groups, one without (n=9) and one with beta-adrenergic blockade by Practolol (n=12). Plasma renin activity increased significantly during halothane anaesthesia alone whereas the surgical manipulations did not further influence mean values significantly. Thus, it seems to be established that anaesthesia per se influences renin secretion. On the other hand Practolol does not show an inhibiting effect. The plasma renin increase following anaesthesia is due to the hemodynamic including renal hemodynamic, changes as well as to activation of the sympatho-adrenal system. Changes in plasma aldosterone are variable. For the greater part of patients with beta-adrenergic blockade an increase during the operative procedure was found. However, in some patients especially in the control group, plasma aldosterone was unchanged or decreased in spite of increasing renin values. Significantly lower plasma potassium concentration in these cases seems to indicate the important contributing role of potassium for the short-term regulation of aldosterone secretion. Plasma sodium concentration remained unchanged for the periods studied.

Adolescent↗
PubMed1975

A study of some beta-adrenoceptor blocking agents on skeletal muscle.

The effect of three recently introduced beta-adrenoceptor blockers practolol, USVC 6524 and Inpea was studied on various skeletal muscle preparations. Practoloo, USVC 6524 and Inpea produced a dose related inhibition of acetylcholine induced contractions of rectus abdominis muscle of frog. These drugs also blocked neuromuscular transmission when tested on in vitro rat phrenic nerve diaphragm preparation; the blockade was partially reversed by physotigmine, KCl and adrenaline and was potentiated by d-tubocurarine. In gastrocnemius sciatic muscle-nerve preparation only Inpea exhibited neuromuscular blocking activity, while practolol and USVC 6524 did not show any effect up to a dose of 10 mg/kg (intraarterially). The apparent discrepancies between the results of in vitro and in vivo experiments could not be adequately explained. It has been discussed that the neuromuscular blockade caused by presently investigated beta-adrenoceptor blocking agents is essentially due to curare-like activity and to a small extent may be due to local anaesthetic activity.

Acetylcholine↗
PubMedDate not supplied

Central action of beta-adrenoceptor antagonists on blood pressure after acute administration in rats.

The effect of an i.v. administration of some beta-adrenergic blocking drugs on blood pressure has been investigated in rats after blood-brain barrier (BBB) opening. Practolol and atenolol which do not penetrate the BBB, induced an immediate hypotensive effect after BBB breakdown by intracarotid (i.c.) injection of cetrimonium. In 39 week-old spontaneously hypertensive rats, practolol (15 mg/kg i.v.) and atenolol (3 mg/kg i.v.) induced a large drop in blood pressure while only a slight decrease was shown in normotensive ones. Likewise, acebutolol induced a significantly greater hypotension after BBB damage. On the other hand, the effects of dl-propranolol (5 mg/kg), quinidine (2.5 mg/kg) and isoproterenol (3 micrograms/kg) on blood pressure were not modified by pretreatment with cetrimonium i.c., while the hypotension induced by d-propranolol (5 mg/kg) was shortened. These results indicate that beta-adrenergic blocking agents with a low degree of lipophily can induce a hypotensive effect when their penetration into brain is largely enhanced after BBB opening either by prolonged hypertension or by cetrimonium. This effect is only dependent on their action on beta-adrenoreceptors; membrane stabilizing effect and intrinsic sympathomimetic activity do not seem to be involved.

Acebutolol↗
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↗
PubMed1978

Effects of indenolol (YB-2), a new beta-adrenergic blocking agent, and its dextro isomer on the central nervous system of mice and rabbits.

Central depressant actions of a new beta-adrenergic blocking agent, indenolol (YB-2), and its dextro isomer were studied in mice and rabbits. d-Indenolol was less active than dl-indenolol in lowering of methamphetamine group toxicity and calming of fighting behavior, though muscle relaxant, hypolocomotive and anticonvulsant effects of d-indenolol were virtually equal to those of the racemate. dl-Propranolol showed a similar profile of central depressant actions to dl-indenolol, whereas dl-practolol revealed no significant central effects in mice. The dose-response relationship between beta-blocking and central effects in the same animal species suggested that both taming and anti-methamphetamine group toxicity effects of dl-indenolol s.c. do not directly relate to either the peripheral beta-blocking or the membrane stabilizing activity. Intravenous as well as intracerebroventricular administration of dl-indenolol resulted in suppression of pressor responses to the electrical stimulation of the brain stem of unanesthetized rabbits. Neither d-indenolol nor dl-practolol was effective against the pressor responses, suggesting that these two compounds acted on the CNS in a manner different from dl-indenolol even when intracerebroventricularly administered. A possible central beta-adrenergic blocking effect of dl-indenolol was discussed in the light of mechanisms of an antihypertensive action of this compound.

Adrenergic beta-Antagonists↗
PubMed1986

Changes of small bowel motility and noradrenaline content of the intestinal wall in response to alpha- and beta-adrenergic blockade in dog.

In experiments on dogs, the spontaneous movements of the small bowel were in all cases enhanced by the alpha 2-blocker phentolamine, while they were not influenced, or were slightly decreased, by the beta 1-blocker practolol. Neither drug caused a change in the noradrenaline content of the intestinal wall. In the same animals, the joint administration of phentolamine and practolol led to a considerable increased small bowel motility, and to a significant decrease in the noradrenaline level of the intestinal wall. The results are in agreement with experimental data indicating that presynaptic alpha-receptors play a primary role in the sympathetic regulation of small bowel motility.

Animals↗
PubMed1975

[Comparison of the pA2 of various beta blocking agents].

The drug industry is now putting out specific beta 1 or beta 2 beta-blocking agents. The pA2 of various beta-blocking agents were determined on isolated organs-guinea pig atrium and trachea: practolol and acebutolol were considered as specific beta-1 inhibitors; butoxamine was a specific beta-2 inhibitor, while pindolol, oxprenolol, propranolol and alprenolol were specificity free. The pA2 quantifies the action exerted by an inhibitor. Cardioselectivity is expressed by the pA2 left atrium/pA2 trachea ratio. It exceeds 1 000 for practolol, it equals 30 for acebutolol, and is very slight for butoxamine. The pA2 therefore gives a good idea of the potential of the various drugs on the animal's isolated organ. However, these data cannot safely be extrapolated to man. Hence the necessity of conducting clinical pharmacological studies.

Acebutolol↗
PubMed1975

[Effects of adrenergic blockade on adipose tissue lipolysis provoked in cats and humans by intravenous perfusion of isoprenaline].

An intravenous infusion of isoprenaline (1 mug/kg/mn during 4 h) elicited a rise in serum free fatty acids (FFA) and glucose in anaesthetised cats. The effect reached a peak in 1 h and was then maintained at a plateau level for the remainder of the infusion. Acebutolol and practolol (0,1-10 mg/kg, p.o.) were more potent in reducing the concentration of free fatty acids (FFA) than in lowering glucose. Propranolol was roughly equipotent on FFA and glucose. In 6 fasted human volunteers, an intravenous infusion of isoprenaline (0,03 mug/kg/mn during 15 min) stimulated a rise in serum FFA. Peak values were attained rapidly and FFA levels began to fall soon after the end of the infusion. Blood glucose concentration was not changed. A placebo, given after the first infusion of isoprenaline, did not significantly affect the response to 2 further infusions at 2 and 4 h later. An oral dose of acebutolol (300 mg) largely suppressed the lipolytic effect of the 2nd and 3rd isoprenaline infusions, the degrees of inhibition being 70 p.cent and 85 p.cent respectively. The same dose of practolol was considerably less effective in inhibiting lipolysis (37 p.cent and 25 p.cent inhibition).

Acebutolol↗
PubMed1974

[Effects of selective beta adrenergic block on myocardial contractility. Relative role of negative inotropic and chronotropic effects].

Left ventricular function was studied in 15 patients both before and after intravenous administration of Practolol (an agent blocking selectively the heart beta-adrenergic receptors (beta 1)), while the heart rate was constant by right atrial pacing. The negative inotropic effect linked to the negative chronotropic effect of the beta-adrenergic blockage, represented approximately one quarter of the overall depression of the contractility. Right atrial pacing determined a decrease of the left ventricular end-diastolic pressure and an increase of the pacing rate by 20% above the spontaneous heart rate, after administration of 30 mg of Practolol, brought the contractility back to its control level.

Arrhythmias, Cardiac↗
PubMed1979

Distribution and characterization of the adrenoceptors in dog coronary arteries.

Effects of catecholamines were studied in vitro on different portions of the left coronary artery of the dog. Adrenaline, noradrenaline and isoprenaline produced dose-related contractions in the common portion of the coronary artery which were blocked by phenoxybenzamine. The proximal portions were relaxed by noradrenaline and isoprenaline, but contracted or relaxed by adrenaline following an initial transient contraction. The contraction was blocked by phenoxybenzamine and the relaxation was blocked by propranolol. Adrenaline, noradrenaline and isoprenaline caused only relaxations which were blocked by propranolol in the distal portion and in the small branches. In coronary, femoral and tracheal strips contracted previously by KCl with or without a phenoxybenzamine pretreatment, isoprenaline produced dose-dependent relaxations. The dose-response curves for isoprenaline were shifted to the right on treatment with practolol. The blocking effects of practolol were nearly ten times potent in the coronary artery in comparison with the femoral artery and the trachea. The results indicate that the common portion mainly possesses alpha-adrenoceptors, the proximal portion contains both alpha- and beta-adrenoceptors, and that beta-adrenoceptors dominate in the distal portion and small artery branches. It is also shown that the beta-adrenoceptors in the coronary vessels differ from the femoral and tracheal beta-adrenoceptors in pharmacological feature.

Animals↗