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At least 1,261 records · Page 70Linked to original sources
PubMed1990

[Effect of Chinoin-103 on K(+)-activated pNPPase in the rat heart].

Effect of a new beta receptor blocking agent, an aryl oxybutanolamine derivative, the Chinoin--103 on K(+)-activated pNPP-ase activity has been studied. Propranolol and practolol were used as reference substances. It has been established that Chinoin-103 in concentration of 10(-4) M significantly hindered total pNPP-ase activity. On the other hand base pNPP-ase activity did not significantly change on the effect of the highest investigable concentration. Study of enzyme kinetic parameters has shown that decrease of base pNPP-ase activity can be attributed to decrease of reaction rate (Vmax decreases) at the same time enzyme affinity to pNPP substrate significantly increases (Km decreases). Taking into consideration the structural similarity of propranolol and Chinoin--103 it is presumable that Chinoin--103 can interact with components of membrane like propanolol and impediment of pNPP-ase activity can be attributed to the interaction.

4-Nitrophenylphosphatase↗
PubMed1977

The effect of beta-adrenoceptor antagonists on the alpha-adrenoceptor blockade produced by phenoxybenzamine.

The effect of beta-adrenoceptor antagonists on the irreversible alpha-adrenoceptor blockade produced by phenoxybenzamine was studied in dogs. The pressor effects of adrenaline were revived after the inhibition by the alpha-receptor block by (+/-) propranolol, (-) INPEA, (+/-) MJ 1999 and (+/-) butoxamine. The enantiomers (+) propranolol and (+) INPEA were ineffective in this regard. (+/-) Practolol also did not revive the pressor effect of the amines. The alpha-receptor mediated effect of the amines, in the nictitating membrana-receptor blockade. It is concluded that (1) blockade of the peripheral (beta-2) receptors is essential for the revival of the pressor effects, (2) local anesthetic effect of the beta-antagonists is not involved. Further work using a series of doses of agonists and antagonists of alpha-and beta-receptors is indicated to clarify the nature of this drug-interaction.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

[Mechanism of the antianginal action of oxyfedrine].

Oxyphedrine was found to depress the tonicity of coronary vessels, increase the coronary circulation volume, the oxygen uptake by the heart and also to exert a positive inoand chronotropic action in test with urethan and cloralose anesthetized cats. These effects were caused by stimulation of the beta-adrenoreceptors of the heart and vessels. In non-anesthetized cats oxyphedrine did not produce tachycardia. Furthermore, under certain conditions (when superimposed on a preliminary administration of practolol- a beta-blocking agent) oxyphedrine can exert a direct inhibitory action on the myocardium.

Adrenergic beta-Agonists↗
PubMed1977

beta-blocking agents and human fat cell adenylate cyclase.

The effects of various beta-blocking agents upon the catecholamine-activated adenylate cyclase of human fat cell ghosts were studied. Both non-selective and cardio-selective beta-blocking drugs are capable in inhibiting the human enzyme system. The concentrations of the non-selective beta-blockers (bupranolol, alprenolol, propranolol, 4-hydroxypropranolol, prindolol and oxyprenolol) required to produce half maximal inhibition of isoproterenol-stimulated rates of cAMP-formation were found to be in a narrow range (5X10(-7) M-3X10(-6) M).The cardioselective beta-blocking agents, however, were only 1/100 (methypranol) to 1/1000 (atenolol, practolol) as potent as the non-selective drugs.

Adenylyl Cyclases↗
PubMed1978

The beta-adrenoceptor controlling renin release.

The beta-adrenoceptor antagonists, atenolol, metoprolol and propranolol, administered intravenously to anaesthetized rats in doses producing equal beta1-adrenoceptor blocking effects, caused comparable suppression of plasma renin activity (PRA) despite the fact that, at these doses, atenolol and metoprolol exhibited no beta2-adrenoceptor blocking properties. Practolol, an agent specific for beta1-adrenoceptors but possessing intrinsic sympathomimetic activity, caused less marked suppression of PRA. When doses of atenolol, metoprolol, propranolol and butoxamine were selected to achieve equal beta2-blocking effects, PRA was again significantly suppressed by atenolol and metoprolol but not by propranolol or butoxamine. These results do not support the concept that adrenergic release of renin is mediated by beta2-adrenoceptors, but are compatible with the involvement of a beta1-adrenoceptor-mediated mechanism.

Angiotensin II↗
PubMedDate not supplied

Reduced beta adrenergic responsiveness in isolated rabbit atria during hypothermia.

Beta adrenergic agonist isoprenaline (8x10(-6)M) produced a 500% increase in inotropic and 90% increase in the chronotropic responses of isolated rabbit atria at 37 degrees C. On cooling the atria to 23 degrees C, these responses were significantly reduced to 87% and 30% respectively. Similar results were obtained with adrenaline, but isoprenaline was more potent. The positive chronotropic and inotropic responses to isoprenaline were effectively blocked by propranolol and practolol at 37 degrees C whereas at 23 degrees C these beta blockers were unable to block even minor positive responses obtained by isoprenaline at this temperature. On the contrary at 23 degrees C, phenylephrine (alpha adrenergic agonist) produced marked positive chronotropic and inotropic effects indicating enhancement of alpha adrenoceptor activity at lower temperatures. This also suggests that reduced beta receptor activity at lower temperature is not due to a generalised depression of adrenoceptors as a result of hypothermia. Rewarming of atria to 37 degrees C restored the beta adrenoceptor responsiveness to previous level. It appears that ambient temperature is important im maintaining normal beta adrenergic activity of the atria.

Animals↗
PubMed1975

Effect of hypoxemia on responses to norepinephrine and angiotensin in coronary and muscular vessels.

The purpose of this study was to determine the relative effects of acute hypoxemia on constrictor responses to norepinephrine and angiotensin in two vascular beds, the coronary and skeletal muscle. The left circumflex coronary and gracilis muscle arteries of anesthetized dogs were perfused at constant flow. Practolol or propranolol was administered to block indirect myocardial effects of norepinephrine on coronary resistance. When Po2 of arterial blood perfusing the coronary and muscle beds was reduced from 101 to 44 mm while systemic Pco2 remained normal, constrictor responses to both norepinephrine and angiotensin were inhibited in coronary vessels but not in muscle vessels. When local Po2 was reduced to 27 mm Hg, inhibition of responses was again observed in the coronary circulation with both drugs; in the muscle, responses to angiotensin but not to norepinephrine were depressed significantly. Since intracoronary infusion of adenosine increased, rather than inhibited, vasoconstrictor responses to angiotensin, it is unlikely that release of adenosine during hypoxemia accounts for inhibition of vasoconstriction in the coronary circulation. Indomethacin did not alter the inhibition of coronary vasoconstrictor responses to angiotensin during hypoxemia, which suggests that releease of prostglandins during htpoxemia is not the primary mechanism for inhibition of coronary vascular responses. When contractions in the gracilis muscle were produced by electrical stimulation, vasconstrictor responses to norepinnephrine were inhibited during hypoxemia. We conclude that depression of constrictor responses by hypoxemia is more pronounced in the coronay circulation than in resting muscle, but when muscle is contracting, vasoconstrictor responses are impaired during hypoxemia.

Adenosine↗
PubMed1986

Pharmacodynamic models of various beta blockers: an explanation for the long duration of action of bopindolol.

Models describing the time course of effects (pharmacodynamic models) of various beta blockers in man are used to explain the long duration of action of bopindolol. No matter what effect is used [reduction in exercise heart rate (RER) or isoproterenol dose ratio (DR)] human data show clearly that bopindolol is very potent compared to other beta blockers such as atenolol, metoprolol, pindolol, practolol, and propranolol. In pharmacokinetic terms, however, these drugs show no pronounced difference in their elimination half-life (ranging between 4 and 8 h). Also the site of action of the therapeutic effects (beta 1 receptors) is obviously identical for all beta blockers. Furthermore, there is no evidence to suggest that bopindolol (the prodrug) or hydrolyzed bopindolol (the active substance) is further metabolized to a slowly eliminated active metabolite. Thus, drug disposition provides no argument to explain the long-lasting effects of bopindolol as compared other beta blockers. The long duration of action of bopindolol seems to reflect an usually flat plasma concentration-response curve.

Adrenergic beta-Antagonists↗
PubMed1989

Differential coupling to positive inotropic responses of cyclic AMP produced by stimulation of beta 1- and beta 2-adrenergic receptors.

In canine right ventricular muscle, isoproterenol, a nonselective beta-agonist, and T-1583, a selective beta 1-agonist, produced positive inotropic effects (PIE) as full agonists. Their PIEs were antagonized by atenolol, a selective beta 1-antagonist, (pA2 = 7.71 for isoproterenol and pA2 = 7.82 for T-1583). The PIE of T-1583 was also antagonized by practolol, a selective beta 1-antagonist (pA2 = 6.55). Procaterol known as a selective beta 2-agonist gave a biphasic concentration-response curve with a maximum that was approximately half those of isoproterenol and T-1583. The PIE of procaterol at low concentrations (pD2 = 7.93), which maximum was approximately 10% of the maximum of isoproterenol, was antagonized by ICI 118,551, a selective beta 2-antagonist (ICI; pA2 = 8.84) and that at high concentrations (pD2 = 5.12) by atenolol (pA2 = 7.56). Increases in cyclic AMP content produced by isoproterenol were reduced greatly by atenolol and slightly by ICI, whereas those produced by T-1583, which were smaller than those by isoproterenol, were abolished by atenolol but not changed by ICI. Procaterol (10(-7) M) produced an increase in cyclic AMP, which was abolished by ICI but not changed by atenolol, to almost the same extent as procaterol (10(-5) M) did, which was abolished by atenolol and slightly reduced by ICI. These results indicate that increased cyclic AMP through beta 1- but not beta 2-receptors couples well to PIE.

Adrenergic beta-Antagonists↗
PubMed1989

Flecainide and cardiac dysrhythmias during dental extraction under anaesthesia.

In a randomized double-blind study, either oral flecainide acetate 400 mg (a Class IC anti-dysrhythmic drug) or placebo was given in two divided doses 12 and 2 h pre-operatively to 38 patients undergoing outpatient molar extractions under halothane anaesthesia. The ECG was continuously monitored from the patients' arrival at the out-patient theatre until discharge, using a two-channel ambulatory magnetic tape recorder. There was a much lower incidence of ventricular dysrhythmias in patients who received flecainide (22%) than those who received placebo (75%) (P less than 0.05). In addition, dysrhythmias were both more severe and more prolonged in the untreated group, prompting treatment with intravenous practolol in seven patients (35%). Flecainide was well tolerated and no adverse effects were reported.

Adolescent↗
PubMedDate not supplied

[Experimental studies of the specificity and aspecificity of a beta-adrenolytic agent, bunitrolol (Kö 1366)].

In basis of our experimental researches bunitrolol presented: a) beta-adrenolytic activity prevailingly at cardiac level (superior to propranolol and practolol) in respect to vascular, tracheal, bronchial, uterus, intestinal and metabolic level; b) beta-adrenergic intrinsic activity; c) local anesthetic activity; d) chinidino-like activity; e) antiarrhythmic activity; f) hypotensive activity with interferences at the level of vasomotor centres, of the barosensitive zones, of the renin secretion and of the purinergic periphery.

Animals↗
PubMed1989

[Drug-induced pemphigus diseases].

An overview is given on pemphigus diseases induced by certain drugs. Well known inducers are D-penicillamine, and pyritinol-chlorhydrate. Besides that in some rather rare cases other drugs were connected to pemphigus induction: rifampicin, INH, etambutol, practolol, propranolol, phenylbutazone, aurothiomalate, ibuprofen, heroin, penicillin, ampicillin, captopril, thiopromine, alpha-mercaptopropionylglycine and piroxicam.

Drug Eruptions↗
PubMed1989

Atenolol-induced cutaneous vasculitis.

We present a case of cutaneous vasculitis apparently due to an adverse reaction to atenolol. The causal relationship between the drug and the eruption was based mainly on circumstantial evidence. It has been further strengthened by positive results of the indirect rat mast cell degranulation test. The number of published cases of reaction to atenolol is limited. Cutaneous vasculitis has, to the best of our knowledge, never been reported as an adverse reaction to atenolol, although it is not a rare side effect of other beta blocker drugs including propranolol and practolol. Atenolol should be added to the list of beta blocker medications that may produce cutaneous vasculitis.

Atenolol↗
PubMedDate not supplied

Demonstration of beta 1-adrenergic receptors in human placenta by (-)[125I]iodocyanopindolol binding.

The highly specific beta-adrenergic radioligand (-)[125I]iodocyanopindolol (ICYP) was used to characterize the beta-adrenergic receptor subtype present in human placenta. Binding of ICYP to membranes from human placenta was saturable with time and ligand concentration, of high affinity, and demonstrated appropriate stereoselectivity and agonist rank order of potency for binding to a beta-adrenergic receptor. From saturation binding curves, the KD and Bmax values for ICYP binding were 233 +/- 51 pM and 690 +/- 139 fmol/mg of proteins, respectively. Analysis of inhibition of ICYP binding by beta 1- and beta 2-selective adrenergic antagonists via Hofstee analysis resulted in linear plots, indicating the existence of a homogeneous population of beta-adrenergic receptors. From the resulting KI-values for the beta 1-selective drugs practolol (4.0 +/- 0.9 microM) and metoprolol (0.19 +/- 0.07 microM) and for the beta 2-selective drug ICI 118,551 (0.30 +/- 0.06 microM) it is concluded that the beta-adrenergic receptor in human placenta is of the beta 1-subtype. This is further supported by the fact that (-)-noradrenaline and (-)-adrenaline were equipotent in inhibiting ICYP binding.

Female↗
PubMed1989

[Beta1- and beta2-adrenergic effects on thrombocytopoiesis in rats].

The influence of beta 1- and beta 2-adrenergic agent injections to rats during 3 days, on the main parameters of thrombocytopoiesis: platelet number and per cent of build up 75seleno-methionine in newly-formed platelets of rats has been studied. It is established that beta 1-adreno-stimulation with dobutamine (DB) increases both the number of platelets and the per cent of build up isotope. Practolol (PC), a beta 1-adrenergic blocking agent, used separately, and combined application of PC + DB lowered significantly the parameters studied. Salbutamol stimulation of beta 2-adrenergic receptors induced an insignificant rise in the thrombocytopoiesis parameters. beta 1-adreno-stimulation with DB results in activation, while beta 1-adrenoblocking with PC--in suppression of thrombocytopoiesis. Pretreatment with PC prevents DB stimulating effect on thrombocytopoiesis, thus evidencing the beta 1-adrenoceptor dependence on the process.

Adrenergic beta-Agonists↗
PubMed1989

[A study on mechanism of skin penetration by cercaria of S. japonicum and screening of preventive drugs].

Mice pretreated with PG cyclo-oxygenase inhibitor aspirin, at 300 mg/kg/d x 5, and ibuprofen, at 100 mg/kg/d x 5 orally and 20 mg/kg/d x 3 intraperitoneally revealed moderate chemoprophylactic effects and the reduction of the penetration of worms by 23% when compared to controls. Daily oral administration of aspirin, at 300 mg/kg for 15 days the worms reduction increased to 41.7%. In estimation of PGE1 in cercariae of S. japonicum by radioimmunoassay, the PGE1 was 49 pg/100 cercariae. In normal mouse skin PGE1 has been measured to amount to 3105 +/- 691.7 pg/10 mg on average. In cercarial penetrated mouse skin, 1.5 hours after exposure the PGE1 assessed in 100 and 250 cercariae in the infected skin were 5506 +/- 1127.1 and 12085 +/- 2622.9 pg/10 mg respectively, which were significantly higher than that of the non-penetrated skin. These studies in conjunction with our previous work indicate that: 1.PGs, similar to S. mansoni, were probably necessary for cercarial penetration. 2.PG inhibitors could reduce cercarial penetration. Receptors antagonist etc. e.g. diphenhydramine, chlorpheniramine, atropine, practolol could not reduce cercarial penetration, but praziquantel in the pretreated mice could reduce cercarial penetration significantly. e.g. 400 mg/kg orally 2 hours prior to affection of cercariae about 100% reduction of the penetration, but if pretreated with praziquantel, 4, 8, 24, 36 hours prior to the affection the reduction penetration decreased to 51.7, 46.1, 9.4, 8.9% respectively.

Alprostadil↗
PubMed1987

Alpha- and beta-adrenergic receptors in the horse ureter.

The presence of both alpha and beta adrenergic receptors in the caudal third ureter of the horse were studied in vitro under isometric conditions using adrenergic agonist and antagonist drugs. Isoprenaline and the beta 2- stimulating agent, salbutamol, elicited relaxation of the ureter smooth muscle strips. The responses were not affected by the beta 1- blocking agent, practolol, but were totally abolished by propranolol and the beta 2- blocking agent, butoxamine. The stimulation of alpha-adrenergic receptors with noradrenaline and phenylephrine evoked a contractile effect which was totally inhibited by phenoxybenzamine and the alpha 1- blocking agent, prazosin. It is concluded that in the horse ureter the alpha receptors are dominant and belong to alpha 1 subtype while the beta receptors are recessive and belong to beta 2- adrenoceptor subtype.

Animals↗
PubMed1985

Differential inhibition of beta adrenergic receptors in human and rabbit ciliary process and heart.

Prior biochemical studies have suggested that beta adrenergic receptors in the ciliary process are mostly of the beta-2 subtype. The present experiments evaluate a number of beta adrenergic antagonists, including several recently developed drugs, for their ability to block rabbit and human ciliary process and heart beta adrenergic receptors activating adenylate cyclase. Three of these agents (alpha-methylpropranolol, IPS 339 and ICI 118,551) demonstrated a high degree of oculoselectivity in both rabbit and human. The other agents (S 37-429, S 32-468, ICI 78,462,H35/25, butoxamine, propranolol, timolol, atenolol and practolol) showed either modest or no oculoselectivity. Structure-activity studies suggested that, among antagonists of the aryloxymethyl type, methylation of the side-chain alpha-carbon or the aromatic ring may enhance oculoselectivity primarily by decreasing potency at cardiac beta adrenergic receptors. Additional physiological studies of cardiac chronotropic response revealed that, compared with nonselective beta blockers, compounds with biochemical oculoselectivity demonstrate decreased physiological effects on cardiac function. This was true when the selective agents were applied either systemically or topically to the eye. On the other hand, the systemic absorption of topical timolol was sufficient to block cardiac chronotropic effects completely. These findings, identifying relatively specific blockers of rabbit and human ciliary process beta adrenergic receptors, have implications for the development of ocular hypotensive agents with fewer systemic side effects on tissues enriched in beta-1 adrenergic receptors.

Adenylyl Cyclases↗