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At least 631 records · Page 35Linked to original sources
PubMed1973

Beta-adrenoceptor blocking properties and cardioselectivity of M & B 17,803A.

1. The beta-adrenoceptor blocking properties of (+/-)-1-(2-acetyl-4-n-butyramidophenoxy)-2-hydroxy-3-isopropylaminopropane hydrochloride (M&B 17,803A) have been compared with those of practolol and propranolol in the guinea-pig, cat and dog.2. Following either intravenous or oral administration in the cat or dog, M&B 17,803A and practolol had similar potency in antagonizing isoprenaline-induced tachycardia and both showed cardioselectivity, but both were less potent than propranolol.3. M&B 17,803A and practolol had approximately one hundredth the intravenous potency of propranolol in increasing the severity of anaphylactic bronchospasm in the conscious sensitized guinea-pig.4. M&B 17,803A possessed less marked intrinsic sympathomimetic activity than practolol but, like propranolol, it had significant local anaesthetic properties and increased the refractory period of rabbit isolated atria.

Acetanilides↗
PubMed1982

The influence of drugs on the overflow of noradrenaline and the identification of receptors in guinea-pig atria.

1 Salbutamol (1.0 microM) and isoprenaline (1.2 nM) significantly increased the fractional release of tritiated noradrenaline from driven left atria but phentolamine (10 microM) failed to do so. Butoxamine (4.0 microM) blocked the increase in overflow produced by isoprenaline. Isoprenaline (1.2 nM), phentolamine (10.0 microM) and salbutamol (1.0 microM) failed to increase the overflow of tritiated noradrenaline from spontaneously beating atria. 2 Spontaneously beating atria were therefore used to identify the receptors mediating chronotropism and inotropism. 3 There was no clear relationship between inotropism and chronotropism. 4 The inotropic effects of both dobutamine (0.04-4.0 microM) and isoprenaline (0.11-9.0 nM) were inhibited by practolol (4.0 microM) and by butoxamine (4.0 microM). The chronotropic effects were inhibited only by practolol (4.0 microM). 5 Both inotropic and chronotropic effects of noradrenaline (3.0-200 nM) were antagonized by practolol (4.0 microM), but not by butoxamine (4.0 microM). Thus both functions appeared to be mediated by beta 1-adrenoceptors when noradrenaline was the agonist. 6 Inotropic responses to salbutamol (0.45-7.5 microM) were inhibited by both practolol (4.0 microM) and by butoxamine (4.0 microM), but chronotropic responses were antagonized only by butoxamine (4.0 microM), Thus salbutamol acts on both beta 1-and beta 2-adrenoceptors to produce an inotropic response but only on beta 2-adrenoceptors to produce its chronotropic response. 7 It is concluded that both beta 1- and beta 2-adrenoceptors can mediate chronotropism and inotropism in guinea-pig isolated atria. Determination of the postsynaptic effects of drugs should be carried out on spontaneously beating rather than driven atria to obviate modification of the responses by noradrenaline release from sympathetic neurons.

Albuterol↗
PubMed1995

Blockade of beta-adrenoceptor in control of blood pressure in fowl.

Several avian species show elevated blood pressure (BP) and spontaneous atherogenesis in the aorta and other large arteries. The BP appears to be influenced by age, sex (higher in males), environment, and diet in some species. We reported previously that mean aortic pressure and heart rate, but not plasma renin activity (PRA), of conscious female domestic fowl were markedly reduced by propranolol. In the present study, we aimed to determine in conscious roosters whether 1) hypotension evoked by atenolol or practolol, which selectively inhibit cardiac beta-receptors in mammals, is more potent than that evoked by propranolol, and 2) the renin-angiotensin (ANG) system and/or catecholamines are involved in beta-adrenoceptor antagonist-induced hypotension. Mean arterial pressure (171.2 +/- 3.5 mmHg) and heart rate (281 +/- 4 beats/min) of chronically cannulated roosters (n = 38) were markedly reduced by acute infusion or repeated injections (14 days) of propranolol, atenolol, or practolol, but not by SQ-14,225 (ANG-converting enzyme inhibitor) or [Sar1, Thr8]ANG II (nonselective ANG receptor antagonist). None of the beta-adrenoceptor blockers, however, showed cardioselectivity. The resting PRA of conscious roosters (1.27 +/- 0.09 ng.ml-1.h-1, n = 38) was low and did not change significantly after chronic or acute treatment with beta-adrenoceptor blockers except for a slight decrease induced by practolol. PRA increased after SQ-14,225. The plasma levels (pg/ml) of norepinephrine (701.9 +/- 76.0), epinephrine (337.2 +/- 57.1), and dopamine (299.1 +/- 39.0) of conscious roosters were further increased by propranolol. Practolol also increased dopamine significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1980

Local anesthetic activity of beta-adrenergic blocking drugs in the Crayfish giant axon, with reference to calcium ion.

The actions of beta-adrenergic blocking drugs, propranolol, pindolol, timolol, carteolol, sotalol and practolol, were examined regarding effects on crayfish giant axon in an attempt to determine the relationship among chemical structure and local anesthetic activity, and the interaction of these drugs with Ca++. The activities of local anesthetics such as procaine and lidocaine served for comparisons. A conventional microelectrode technique was used to obtain the resting membrane and action potentials. All drugs except sotalol and practolol dose-dependently inhibited the dV/dt and amplitude of the action potential with a slight decrease (less than 6 mV) in the resting membrane potential. The relative potencies of these drugs in the reduction of the dV/dt were as follows: propranolol 13.3, pindolol 1.7, procaine 1.0, lidocaine 0.91, timolol 0.71 and carteolol 0.22. Sotalol and practolol had little activity. The chemical structure of the drugs for local anesthetic action was closely related to that of the lipophilic aromatic group; the most potent activity seen in the naphthyl group. Potentiation of the local anesthetic activity in low Ca++ solution was obtained with pindolol, timolol, carteolol, sotalol and practolol. Reduction of the activity in high Ca++ solution was observed with propranolol, pindolol, timolol, procaine and lidocaine. These results suggest that external Ca++ competes with the local anesthetic action of the beta-adrenergic blocking drugs, at the site of the action potential generating mechanism.

Action Potentials↗
PubMed1984

Estimation of the nonspecific cardiovascular toxicity of beta-adrenoceptor blocking drugs with different hydrophobic properties in the cat.

The structure-activity relationship between the acute nonspecific cardiovascular depressant effects of the beta-adrenoceptor blocking drugs and their hydrophobic properties was evaluated experimentally for propranolol, pindolol, practolol, and atenolol, in the anaesthetized cat after preceding beta-adrenoceptor blockade. The LD50 values (geometric mean and range in mumol/kg i.v., each drug n = 5) for the nonspecific depression of max dp/dt were: 7.5 (5.6-9.1) for propranolol, 21 (15.5-28) for pindolol, 190 (115-290) for practolol, and 230 (170-400) for atenolol. The respective partition coefficients in octanol buffer (pH 7.0) as a measure of hydrophobicity were: propranolol 5.4, pindolol 0.20, practolol 0.025, and atenolol 0.0032. These experimental data showed a good fit into the regression equation obtained previously [18]. Practolol, in contrast, had a lower toxicity than calculated because of a pronounced intrinsic sympathomimetic activity (ISA), even after catecholamine depletion. The nonspecific cardiovascular toxicity of 15 other clinically used beta-adrenoceptor blocking drugs were estimated from their respective octanol buffer partition coefficients. The fall of the diastolic blood pressure was representative of the toxicity of the compounds. It is concluded that the cardiovascular toxicity is lowest in compounds with low hydrophobicity and with distinct ISA.

Adrenergic beta-Antagonists↗
PubMed1987

The effect of beta blockers on cardiac neural discharge associated with coronary occlusion in the cat.

The effect of timolol on postganglionic cardiac sympathetic neural discharge, blood pressure, heart rate, and rhythm changes associated with acute coronary occlusion of the left anterior descending artery was examined and compared with the effects of the beta blockers practolol and metoprolol. Timolol (5 mg/kg, IV) was infused 15 minutes prior to coronary occlusion in cats anesthetized with alpha-chloralose. Control heart rate fell from 129 +/- 10 to 106 +/- 2 one minute prior to coronary occlusion and remained at 106 +/- 2 beats/minute in the minute prior to arrhythmia. Control blood pressure fell from 126 +/- 20 to 91 +/- 19 and stabilized at 99 +/- 19 mm Hg one minute prior to coronary occlusion. Mean time to arrhythmia and death was 4.7 +/- 2.3 and 68.0 +/- 51.0 minutes (P greater than .05 vs no drug), respectively. Three cats died and two were sacrificed six hours after coronary occlusion. Blood pressure fell to 86 +/- 20 mm Hg two minutes after coronary occlusion, rose to 95 +/- 23 mm Hg at ten minutes, and remained there for ten minutes. Timolol did not alter postganglionic cardiac sympathetic neural discharge prior to coronary occlusion. Two minutes after coronary occlusion, mean postganglionic cardiac sympathetic neural discharge was 128 +/- 27 and increased to 139 +/- 36 impulses/second (% control) 4 minutes after coronary occlusion. A similar trend was found for the data recorded in 15 nerves (eight cats) in which coronary occlusion was initiated without timolol. The data suggest that a difference exists among beta blockers because prior to coronary occlusion, the cardioselective drugs metoprolol (1, 5, and 10 mg/kg, IV) and practolol (8 mg/kg, IV) depressed postganglionic cardiac sympathetic neural discharge whereas noncardioselective timolol did not. Because all three beta blockers increased the times to arrhythmia and death (although the increase was significant only after metoprolol and practolol), the acute protective mechanism does not appear to be due primarily to a depression of spontaneous sympathetic neural discharge.

Adrenergic beta-Antagonists↗
PubMed1983

The effect of cardiac denervation and beta-blockade on control of cardiac output in exercising dogs.

Normal and cardiac denervated dogs, with an electromagnetic aortic flowprobe implanted at least 14 days before the experiments, ran at different speeds on a 25% graded treadmill. The experiments were carried out before and after blockade of betareceptors in the heart by PO administration of 125 mg X kg-1 practolol per day. Changes in stroke volume, heart rate, and cardiac output were measured. After beta-adrenergic blockade, only two of the seven dogs with denervated hearts were prepared to run at a limited number of speeds. Time constants of the cardiac output changes at the onset of exercise were significantly different (P less than 0.001) for the normal (11.5 +/- 0.7 s, mean +/- SEM) and the denervated dogs (29.5 +/- 1.1 s), but in normal dogs did not change with practolol (11.8 +/- 0.8 s). The steady state relationship between cardiac output (CO) and work per unit time performed on the treadmill (P) was for normal dogs: CO = 156 + 1.55P, for normal dogs after practolol treatment: CO = 156 + 0.43P (slope significantly different, P less than 0.05), and for dogs with denervated hearts: CO = 121 + 2.06P (not significantly different from normal dogs). It was concluded that changes in the venous or arterial system alone are not sufficient to increase cardiac output appreciably during exercise. The magnitude of the cardiac output increase depends more on the presence of intact beta-receptors than on the presence of intact cardiac nerves.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

Studies on the positive inotropic effect of dopamine in the guinea-pig heart.

The positive inotropic effect of dopamine has been studied in isolated ventricular strips of guinea-pig heart. The concentration-inotropic response curve for dopamine was significantly shifted to the right by pretreatment with reserpine. In preparations obtained from animals pretreated with reserpine (2.5 mg/kg, 24 h prior to the experiment) the dose-response curve was not significantly affected by haloperidol, a dopamine vascular receptor antagonist (10(-6)-3X10(-6) M). The inotropic effect of dopamine was antagonized by practolol (3X10(-7)-10(-6) M), but not by phentolamine (3X10(-6)-10(-5) M); moreover the alpha-adrenoceptor blocking drug (10(-5) M) did not affect the curve for dopamine in the presence of practolol (3X10(-7) M). In preparations in which fast sodium channels were blocked by K+ -rich medium, slow electrical responses (calcium-mediated action potentials) as well as contractions were induced by high concentrations of dopamine (10(-4)-3X10(-4) M); again these responses were unaffected by phentolamine or haloperidol, but were blocked by practolol. It was concluded that in the guinea-pig ventricular muscle dopamine induced a positive inotropic effect through both indirect and direct action, and that the latter is due to the activation of beta-adrenoceptors.

Animals↗
PubMed1986

The positive inotropic response to milrinone in isolated human and guinea pig myocardium.

The bipyridine derivative, milrinone, produced positive inotropic effects in isolated, contracting right ventricular papillary muscles and left atria from guinea pigs as well as in human papillary muscle strips. The inotropic effect was biphasic in guinea pig papillary muscles (EC50, high affinity, 1.5 X 10(-6) mol/l, about 35% of maximal effect; apparent EC50, 3 X 10(-5) mol/l with a maximal effect at 2 X 10(-4) mol/l) but monophasic in guinea pig left atria (EC50, 6 X 10(-5) mol/l) and in human papillary muscle strips (EC50, 5.8 X 10(-5) mol/l). In guinea pig papillary muscles, reserpine pretreatment or l-practolol preincubation reduced the low concentration effect only. In the presence of l-practolol, carbachol reduced the low concentration effect only. In the presence of l-practolol, carbachol reduced but not abolished the inotropic effects of milrinone (3 X 10(-6) mol/l, 1 X 10(-4) mol/l) in both guinea pig and human myocardium. This antagonism was prevented by atropine preincubation. The maximum inotropic effect of milrinone was similar to that of ouabain and calcium in guinea pig myocardium but markedly less than either calcium or ouabain in human myocardium. Milrinone inhibited crude guinea pig and human cardiac phosphodiesterase activity in vitro but did not inhibit 3H-ouabain binding to partially purified human cardiac (Na+ + K+)-ATPase-containing membranes. We conclude that the primary mode of action of milrinone in both guinea pig and human myocardium is through inhibition of phosphodiesterase.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1977

Treatment of hypertension successively with a diuretic, clonidine or a beta-blocking agent and hydralazine.

The present study was carried out in an homogenous group of 49 untreated hypertensive patients, all aged 45 years. Diastolic blood pressure was equal to or greater than 110 mmHg in successive measurements; eleven patients were classified as WHO group II, and the others as WHO group I. An initial placebo period of 3 weeks was followed by cyclothiazide medication with a good response in 6 patients. The remaining patients were given either clonidine or practolol, and by adjustment of the dose a good response was obtained in 31 patients. In these cases the treatment was exchanged after 6 weeks. The antihypertensive effect of relatively small doses of clonidine was equal to that of practolol. Since completion of the study practolol has been withdrawn because of the emergence of long term toxic effects. In 12 cases, hydralazine had to be added to obtain a satisfactory response. Mild side-effects were common, especially at the beginning of clonidine treatment, but they did not necessitate discontinuation of treatment. Further comparative studies of clonidine and beta-blockers should be carried out and more experience with the combination of clonidine and vasodilators in the treatment of hypertension is necessary.

Benzothiadiazines↗
PubMed1979

Long-term haloperidol-treatment of mice: a change in beta-adrenergic receptor responsiveness.

Mice administered haloperidol 3 mg/kg/day in their drinking water for 21 days were tested for their locomotor responsiveness to saline or acid vehicle, dl-, l- or d-propranolol, metoprolol, butoxamine or practolol. Haloperidol-treated animals administered saline or acid-vehicle were, in five of six experiments, more active than animals withdrawn from vehicle-treatment. Haloperidol- and vehicle-treated animals responded differently to the non-selective beta-adrenoreceptor antagonists (dl-propranolol and l-propranolol) and selective beta1-adrenoreceptor antagonists (practolol and metoprolol), but not to a selective beta2-adrenoreceptor antagonist (butoxamine). With dl-propranolol (4 mg/kg) the locomotor activity of haloperidol-treated animals was significantly (0.01 less than P less than 0.02) greater than that of the vehicle-treated animals. Similar effects in the same direction were seen with l-propranolol (1 mg/kg, 0.005 less than P less than 0.01), practolol (10 and 100 mg/kg, 0.025 less than P less than 0.05 and 0.01 less than P less than 0.025 respectively) and metoprolol 8 mg/kg, 0.005 less than P less than 0.01). The d-isomer of propranolol which is about 50 times less active as a beta-adrenoreceptor antagonist than the l-isomer, although having equal membrane stabilizing effects, did not differentially affect haloperidol- or vehicle-treated groups. The results suggest that there has been a change in beta 1-adrenoreceptor responsiveness in animals withdrawn from long-term haloperidol treatment.

Adrenergic beta-Antagonists↗
PubMed1986

Pharmacological characterization of the receptor mediating the adrenergic inhibition of responses to substance P in the cingulate cortex.

The excitatory responses of neurones in the anterior cingulate cortex of the rat to iontophoretically applied substance P (SP) are reduced by noradrenaline (NA) applied iontophoretically or released from noradrenergic pathways. In order to determine the receptor involved in this inhibitory effect we have studied the effects of a number of receptor-specific adrenergic agonists and antagonists on responses of cingulate neurones to SP in rats anaesthetized with chloral hydrate. Low iontophoretic currents (0-15 nA) of NA, adrenaline and the beta-agonist, clenbuterol, all strongly reduced responses to SP. Isoprenaline was also effective but less consistently so, although problems were experienced with its iontophoretic release from micropipettes. The alpha 1-agonists, phenylephrine and methoxamine were also able to reduce responses to SP. However, this reduction required higher iontophoretic currents (15-60 nA) and was associated with depressant effects on baseline firing rate. The alpha 2-agonist clonidine was only weakly active at high currents and this too was associated with depression of baseline firing. Similar weak effects were noted with dopamine. The inhibitory effects of NA on SP responses were convincingly blocked or reversed by the beta-antagonist, practolol, but not by the alpha 1-antagonist, prazosin. The reduction of SP responses by phenylephrine was also blocked by practolol but unaffected by prazosin. Finally, reduction of SP excitations by activation of the coeruleocortical pathway was also blocked by practolol applied iontophoretically to the cortical cells. These results are consistent with the hypothesis that the effect of NA on SP responsiveness in the cingulate cortex is mediated by beta-adrenoreceptors.

Albuterol↗
PubMed1983

Beta adrenergic receptors and glucagon in seizures from exposure to oxygen at high pressure (OHP).

Previous studies have shown that sympathetic factors and blood glucose are of importance in the development of seizures and lung damage from OHP. In the present study we examined the influence of beta sympathetic agonists and blocking agents and glucagon on OHP toxicity. Rats were exposed to 6 ATA OHP and examined for time-to-seizure and lung damage. Pretreatment with propranolol increased the time-to-seizure by 70% and practolol by 50% without altering gross lung appearance or lung wet wt/dry wt. Propranolol and practolol also prevented brain glycogen depletion prior to seizure which otherwise occurred in subconvulsive exposure to OHP. Isoproterenol and glucagon pretreatment had no effect on time-to-seizure but isoproterenol did increase lung injury. Both practolol and propranolol block the beta-receptor influence on adenyl cyclase-stimulated second messenger production, while both isoproterenol and glucagon activate adenyl cyclase to produce second messenger. Our results may suggest a possible role for second messenger in mediating some of the acute toxic effects of OHP on the CNS.

Animals↗
PubMed1976

beta-receptor-blockade hypotension and the central nervous system.

1. Intravenous infusion of propranolol (3-86 micronmol h-1 kg-1) for 2 h lowered arterial pressure in the conscious rabbit whereas similar infusions of practolol (37-6 micronmol h-1 kg-1) did not. 2. The fall in blood pressure produced by propranolol was accompanied by a decrease in splanchnic nerve activity. Practolol did not change splanchnic nerve activity. 3. A centrally mediated decrease in sympathetic nervous activity makes an important contribution to the hypotensive action of propranolol in the rabbit. This effect is not shown by practolol.

Animals↗
PubMed1979

Comparison of the immediate effects of five beta-adrenoreceptor-blocking drugs with different ancillary properties in angina pectoris.

We compared the immediate effects of five beta-adrenoreceptor-blocking agents in 16 patients with stable angina pectoris. Acute dose-response studies showed that all five drugs improved exercise tolerance and reduced ST-segment depression, heart rate and blood pressure by a similar degree in comparison with a placebo (P less than 0.01). Near maximum improvement in exercise tolerance occurred when the acute cumulative oral dose had reached 160 mg for propranolol and oxprenolol, 200 mg for metoprolol and tolamolol and 400 mg for practolol. When these drugs were administered as a single doses, increase in walking time before the development of angina and reduction in ST-segment depression, heart rate and systolic blood pressure all occurred within one hour and persisted for eight hours--effects markedly different from the response to a placebo (P less than 0.01). These data show that non-cardioselective agents (propranolol and oxprenolol), cardioselective agents (practolol, metoprolol and tolamolol), as well as drugs with intrinsic sympathomimetic activity (oxprenolol and practolol), were equally effective in the treatment of angina pectoris.

Adult↗
PubMed1978

Attempts to attenuate the cardiostimulatory effects of ketamine.

In an attempt to attenuate the cardiostimulatory effects of ketamine, a number of drugs were given individually, or in combination, to fit adults undergoing body surface operations, either before or aftera ketamine induction of 1 mg kg-1 followed by an infusion of 1 mg ml-1. Of these, practolol, phentolamine, practolol-phentolamine, phentolamine-practolol, promethazine, hexamethonium, procainamide and verapamil were unacceptable. Labetalol, in doses of 0.5 mg kg-1 and 1.0 mg kg-1, proved to be the most promising drug and is worthy of further study.

Adult↗
PubMed1988

Effects of beta-adrenoceptor antagonism on the cardiovascular and catecholamine responses to tracheal intubation.

The catecholamine and cardiovascular responses to laryngoscopy and tracheal intubation were studied in 20 patients who underwent elective gynaecological surgery and who were allocated randomly to receive either practolol 10 mg or saline intravenously prior to induction of anaesthesia. Anaesthesia was induced with fentanyl and thiopentone; atracurium was administered and the lungs were ventilated artificially with 67% nitrous oxide in oxygen. Tracheal intubation was performed when muscle relaxation was adequate. Arterial pressure, heart rate, plasma noradrenaline and adrenaline concentrations were measured before and after tracheal intubation. A significant increase in catecholamine concentrations occurred in both groups in response to tracheal intubation but the magnitude of the increase in adrenaline was greater in the practolol group. There were no significant differences in arterial pressure or heart rate changes between the groups. We conclude that pretreatment with practolol is of no value in the attenuation of the hypertensive response to direct laryngoscopy and tracheal intubation in previously normotensive patients.

Adult↗
PubMed1978

Cardiovascular effects of local adrenaline infiltration during halothane anaesthesia and adrenergic beta-receptor blockade in man.

Adrenergic beta-receptor blocking agents, alprenolol, propranolol and practolol were given as a prophylactic measure to patients undergoing middle-ear microsurgery where adrenaline was deliberately infiltrated during halothane-N2O/O2 anaesthesia. These three beta blockers did not differ in their action on heart rate, arterial blood pressure, right ventricular pressure, CVP or peripheral pulse wave in equipotent doses, which were 0.04 mg/kg for alprenolol and propranolol and 0.4 mg/kg for practolol in this study. Atropine caused a highly significant increase in heart rate in the spontaneously ventilating group and maintained blood pressure at higher levels, although the latter difference was not significant. Alprenolol and propranolol offered partial protection for over 40 min against adrenaline-induced arrhythmias. Occasionally occuring tachyarrhythmias were easily terminated with a further dose of a beta blocker. The effective half-life of practolol was less than 15 min and doses up to 0.4 mg/kg were unable to prevent arrhythmias during adrenaline challenge.

Adolescent↗