Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Practolol”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,513 records · Page 84Linked to original sources
PubMed1984

Inotropic drugs and their mechanisms of action.

This report describes various old and new positive inotropic drugs with respect to their mechanisms of action. Drugs with established cardiotonic effects include cardiac glycosides, beta 1-adrenergic agents, glucagon, histamine and the methylxanthines. New agents discussed are prenalterol, beta 2- and alpha-adrenergic drugs, amrinone and sulmazole. Prenalterol is a beta 1-adrenergic agent. Beta 2-adrenergic drugs, amrinone and sulmazole, combine a positive inotropic and a vasodilator effect. The latter resemble theophylline and other methylxanthines in that they appear to act mainly as phosphodiesterase inhibitors with a subsequent increase in cyclic adenosine monophosphate (cAMP). The mechanism of the positive inotropic effect of alpha-adrenergic stimulating agents (for example, phenylephrine) is unknown. It is independent of the cAMP system and is not accompanied by changes in frequency.

Aminopyridines↗
PubMed1986

Antiarrhythmic activity of 17 beta-aminoestratrienes. Comparison of 3-ols and 3-acetates with the corresponding 3-(3-amino-2-hydroxypropyl) ethers.

The antiarrhythmic efficacy of 17 beta-amino- and 17 beta-amino-16 alpha-hydroxyestratrien-3-ols and 3-acetates (group 1) was compared with the efficacy of corresponding 3-[2-hydroxy-3-(isopropylamino)propyl] and 3-[2-hydroxy-3-(tert-butylamino)propyl] ethers (group II), substituents which are usually associated with beta-adrenoceptor blocking activity. Group I compounds exerted potent antiarrhythmic activity against both aconitine-induced arrhythmias in mice and ischemia-induced arrhythmias in rats and reduced the maximum following frequency of isolated guinea pig atria. Electrophysiological studies indicated that their mechanism of action is due to an ability to reduce the fast inward sodium current in cardiac cells (class I antiarrhythmic action). Group II compounds were inactive in the aconitine and atrial tests and electrophysiological studies confirmed that they were devoid of class I activity. However, these compounds, like both class I antiarrhythmic and beta-adrenoceptor blocking drugs, were active against ischemia-induced arrhythmias. Group II compounds, unlike group I compounds, exerted nonspecific beta-adrenoceptor blocking actions, which may account for their activity in the rat test. It was concluded that introduction of the 3-substituted ether group did not confer any advantage over the parent 3-ol or 3-acetate compounds.

Action Potentials↗
PubMed2000

Effect of a calcium-sensitizing agent, levosimendan, on the postcardioplegic inotropic response of the myocardium.

Myocardial contractile function after coronary artery bypass graft surgery is often depressed and may require inotropic support, particularly in patients on treatment with beta-adrenergic and Ca2+ blockers. In view of the increase in cytosolic Ca2+ during early reperfusion, use of Ca2+ sensitizing agents may be preferable to adrenergic agonists for enhancement of contractile function after cardioplegic arrest. The aim of this study was to assess the efficacy of the Ca2+ sensitizer, levosimendan, as an inotrope on the mechanical recovery of hearts after normothermic and hypothermic cardioplegic arrest in the absence and presence of Ca2+ and beta-blockers. Isolated perfused working guinea pig hearts were perfused in the absence or presence of propranolol (10(-6) M) and/or nifedipine (10(-8) M), subjected to 45 minutes of normothermic or 180 minutes of hypothermic cardioplegic arrest, reperfused, and exposed to increasing concentrations of levosimendan (10(-9) to 10(-6) M). Levosimendan (10(-7) to 10(-6) M) has positive inotropic, chronotropic, and vasodilatory effects on normoxic perfused control hearts, as well as during reperfusion after 45 minutes of normothermic cardioplegic arrest. Similar effects were elicited in the presence of the blockers. Levosimendan had no stimulatory effect during reperfusion of hearts subjected to prior hypothermic arrest. Except for the increase in heart rate, the effects of levosimendan on functional performance during reperfusion were comparable with those of adrenaline. Levosimendan elicits a positive inotropic and chronotropic response during reperfusion of hearts after normothermic cardioplegic arrest, both in the absence and presence of Ca2+ and beta-adrenergic blockers.

Adrenergic beta-Antagonists↗
PubMed1983

Cardioselectivity of prenalterol and isoproterenol.

We examined the hemodynamic effects and kinetics of prenalterol, a new beta-adrenoceptor agonist, in 10 normal subjects. There is some doubt whether prenalterol is selective for beta 1 adrenoceptors in animals; therefore, we also compared its cardioselectivity with that of the nonselective agonist, isoproterenol, with respect to heart rate (HR) and blood pressure (BP) responses after inhibition of cardiovascular reflexes with atropine, clonidine, and phentolamine. After intravenous (2.5 mg) and oral (10 mg and 100 mg) dosing, t 1/2 beta was 2 to 3 hr. Oral bioavailability averaged 33% and was independent of dose. Oral prenalterol, 10 mg and 100 mg, increased resting HR, systolic BP, and cardiac index by up to 27% but had no significant effects during graded exercise. Prenalterol infusions were calculated to attain steady-state plasma concentrations of 10, 20, and 40 ng/ml. HR and BP effects of the levels (10.8, 23.6, and 47.4 ng/ml) were compared with those of 0.5, 1.5, and 2.5 micrograms isoproterenol. Before autonomic block, prenalterol increased HR by 10 bpm at the highest dose and mean arterial pressure (MAP) by 10 mm Hg. In contrast, HR rose and MAP fell after isoproterenol. After block, at the highest doses of prenalterol and isoproterenol, there was an average rise in HR of 42 and 27 bpm; BP was almost maintained after the former but fell by 33 mm Hg after the latter. Prenalterol is an inotropic drug that has the effects of a full cardioselective beta-adrenoceptor agonist. Its inotropic effects are evident at doses that have little effect on HR because of the modifying effect of cardiovascular reflexes. The hemodynamic effects are most obvious at rest when sympathetic tone is low.

Administration, Oral↗
PubMed1983

Hemodynamics and leg muscle metabolism at rest and during exercise in young healthy men after prenalterol.

In eight young healthy men the effects of short-term treatment with prenalterol, a new beta-adrenergic agonist, on peripheral hemodynamics and leg muscle metabolism were studied at rest and during exercise at a moderate and a heavy workload. At rest prenalterol treatment significantly increased pulmonary oxygen uptake, heart rate, rate pressure product, and leg blood flow and decreased leg arteriovenous oxygen content difference. During exercise fewer hemodynamic effects of prenalterol were observed. At the moderate workload there was a slight increase in heart rate, but at the heavy workload heart rate fell. Prenalterol raised the arterial concentrations of free fatty acids and glycerol at rest by 70% and 40%, but during exercise these alterations were not present. The plasma levels of epinephrine and dopamine in subjects at rest decreased significantly during influence of prenalterol, but these differences were also abolished during exercise. The leg exchange of metabolites and the concentrations of endogenous muscle metabolites were not influenced by prenalterol, although the lactate concentrations in muscle tended to be lower at rest and during exercise. The results at rest demonstrate that prenalterol in this situation acts predominantly as a stimulator of beta 1-adrenoceptors. During heavy exercise, however, when the endogenous sympathetic tone is high, the beta-stimulating effects are no longer overt and instead reduced heart rate indicates a blocking effect on beta-adrenoceptors. The hemodynamic and metabolic results are concordant with the hypothesis that prenalterol acts as a partial beta-receptor agonist.

Adult↗
PubMed1984

Noninvasive assessment of chronotropic and inotropic response to preferential beta-1 and beta-2 adrenoceptor stimulation.

The relative chronotropic and inotropic activity of preferential beta 1- and beta 2-adrenoceptor stimulation was investigated in seven healthy male subjects in a randomized within-subject, single-blind study. Two doses of beta 1-selective agonist prenalterol (1 mg/hr or 2 mg/hr) and of beta 2-selective agonist salbutamol (300 micrograms/hr or 600 micrograms/hr) were infused intravenously in four separate sessions, with intervals of at least 48 hr between sessions. At each session cuff blood pressure and heart rate (HR) were measured and some hemodynamic information on the inotropic state were derived by echocardiography. Both prenalterol and salbutamol induced increases in HR, but tachycardia was greater after salbutamol, whereas the positive inotropic response to beta-stimulation was greater after prenalterol. At comparable HR rises (prenalterol, from 66.0 +/- 5.5 to 72.2 +/- 4 bpm; salbutamol, from 64.6 +/- 6 to 70.0 +/- 7 bpm), inotropic response seemed to be greater after prenalterol than after salbutamol (systolic blood pressure [SBP]: 133.5 +/- 8 and 120.7 +/- 8 mm Hg; mean velocity of circumferential fiber shortening [Vcf]: 1.54 +/- 0.13 and 1.31 +/- 0.12 c/s; ejection fraction [EF]: 72.4% +/- 5% and 69.5% +/- 4%; stroke index: 47.4 +/- 4 and 41.7 +/- 3 ml/m2). In presence of a chronotropic effect (HR from 64.6 +/- 6 to 70.0 +/- 7 bpm), the low salbutamol dose did not induce any changes in the indices of inotropism (SBP: from 119.2 +/- 6 to 120.7 +/- 8 mm Hg; mean Vcf: from 1.28 +/- 0.11 to 1.31 +/- 0.12 c/s; EF: from 68.1% +/- 5% to 69.5% +/- 4%; stroke index: from 40.2 +/- 3 to 41.7 +/- 3 ml/m2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1981

Adrenergic and cholinergic receptors of cerebral microvessels.

The presence of alpha- and beta-adrenergic and muscarinic cholinergic receptors in cerebral microvessels of the rat and pig was assessed by ligand binding techniques. The results demonstrate the presence of specific binding to alpha 2- and beta-adrenergic receptors but no appreciable specific binding to alpha 1-adrenergic or muscarinic cholinergic receptors. beta-Adrenergic receptors of pig cerebral microvessels are similar to those of the brain and other organs in their binding characteristics to the tritiated ligand and in their stereospecificity of binding to the biologically active isomers of beta-adrenergic agonists. Further evidence derived from the differential potency of binding displacement by the various beta-adrenergic agonists and selective beta 1- and beta 2-adrenergic antagonists indicates that beta-adrenergic receptors of pig cerebral microvessels are mostly of the beta 2-subtype.

Animals↗
PubMed1975

beta-Adrenergic receptors and renin release: studies with beta-adrenoreceptor-blocking agents in the conscious rabbit.

1. Plasma renin activity (PRA) and mean blood pressure were studied in conscious rabbits infused with beta-adrenoreceptor antagonists. 2. Oxprenolol and DL-propranolol each significantly reduced PRA and blood pressure, but prindolol, which had a strong blood pressure-lowering effect, increased PRA. 3. When prindolol was given to animals in which PRA and blood pressure had been reduced by DL-propranolol, PRA returned to control values but blood pressure remained low. Thus the increase in PRA caused by prindolol is not mediated by hypotension. These findings, together with the observation that compound H35/25 reduced PRA without altering blood pressure, suggest that the effects of the beta-adrenoreceptor-blocking drugs on blood pressure are unrelated to their effects on renin release. 4. Studies with D-propranolol and with blocking agents with either beta-1 or beta-2 specificity indicated that the effects of beta-adrenoreceptor blockade on renin are directly dependent upon their action on beta-adrenergic receptors, probably of the beta-2 type.

Adrenergic beta-Antagonists↗