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PubMed1988

Adrenaline stimulates acid production in isolated pig and human parietal cells.

To investigate the mechanisms of adrenergic stimulation of the parietal cell and to study the possible relationship between the stress hormone adrenaline and duodenal ulcer, the effects of adrenaline and various adrenoceptor agonists and antagonists were investigated in parietal cells isolated from pig stomachs and from endoscopic biopsy specimens taken from the gastric mucosa of patients. Parietal cell acid production was assayed by the aminopyrine accumulation technique. Adrenaline as the sole drug showed poor or no stimulatory effect but potentiated histamine-stimulated acid production. In the presence of histamine, beta-adrenoceptor agonists caused a stimulation of acid formation with the potency order isoproterenol greater than adrenaline greater than noradrenaline. The beta-2-selective antagonist ICI118551 was a more potent inhibitor of acid production than both the beta-1 antagonist practolol and the H2-receptor antagonist cimetidine. Studies of (3H)-dihydroalprenolol (DHA) binding to purified parietal cell membranes showed a protein-concentration-dependent and specific binding of 2.2 +/- 0.6 pmol DHA/microgram. Adrenaline increased gastric acid production in both pig and human parietal cells, most likely through a beta-2 receptor on the parietal cell. The adrenaline stimulatory effect in cells obtained from patients with peptic ulcer was more pronounced than in cells from non-ulcer patients, which indicates a possible role of adrenaline in some types of ulcer disease.

Adrenergic beta-Agonists↗
PubMed1979

Effect of beta-blockers on sodium and potassium content of human erythrocytes.

Recently, hyperpotassemia was reported in patients treated with propranolol, but the mechanism has not yet been delineated. We have investigated the effects of various beta-adrenergic blockers and of D-propranolol on the Na+ and K+ distribution intra- and extracellularly in human erythrocytes. K+ loss and Na+ gain by cells was demonstrated at drug concentrations of 10(-4) M or greater. D-Propranolol was more effective than L-propranolol, whereas pindolol was ineffective. Practolol increased Na+ content but did not influence K+. The results suggest that electrolyte redistribution across cell membranes is not a likely explanation for hyperpotassemia in patients treated with propranolol, or for the local anaesthetic effect of this drug.

Dose-Response Relationship, Drug↗
PubMed1976

Tricyclic antidepressant overdosage: experimental studies on the management of circulatory complications.

Tricyclic antidepressant overdosage may be complicated by cardiac arrhythmias, which were sometimes difficult to treat prior to the use of sodium bicarbonate. Experiments have been done with several antiarrhythmics in an attempt to define the optimum treatment. Sodium bicarbonate proved the most effective experimentally and this supports our clinical experience. Physostigmine is a useful second drug, having beneficial effects against arrhythmias and central nervous system manifestations of toxicity. Practolol, although reversing the arrhythmias, tends to cause hypotension. Other drugs tried were less effective.

Acid-Base Equilibrium↗
PubMed1983

Effects of hypercapnia on myocardial contractility in piglets.

The effects of acute hypercapnia on cardiac contractility and their dependence on adrenergic pathways were studied in 27 piglets anesthetized with pentobarbital (30 mg/kg, ip). Aortic pressures and flow, and heart rate were held constant; atropine was used to produce parasympathetic blockade. Hypercapnia was achieved by addition of CO2 to the respirator. In the control group (N = 7) the first derivative of left ventricular (LV) pressure (dP/dtmax) increased significantly following induction of severe hypercapnia (PaCO2 greater than 80 mm Hg; pH less than 7.00). There were no significant changes in LV end diastolic pressure. The magnitude of the positive inotropic responses was unaltered by ganglionic blockade with tetraethylammonium chloride (100 mg) (N = 5). In contrast, no change in LV dP/dtmax was observed during hypercapnia in piglets (N = 15) subjected to beta-adrenoreceptor blockade with practolol (4 mg/kg). Our findings indicate that the increased cardiac contractility during acute severe hypercapnia is not dependent upon the integrity of the neural reflex system. Rather, it is due to adrenal release of catecholamines into the circulation. These animals are highly resistant to the intrinsic cardiac depressant action of hypercapnic acidosis.

Acidosis↗
PubMed1976

Isoproterenol antagonism of cardioselective beta adrenergic receptor blocking agents: a comparative study of human and guinea-pig cardiac and bronchial beta adrenergic receptors.

pA2 values against isoproterenol were determined for a number of cardioselective and noncardioselective beta adrenergic receptor blocking agents using human and guinea-pig isolated atrial and bronchial or tracheal preparations to study possible species differences. No significant differences in pA2 values for propranolol, pindolol, Ro 3-4787, acebutolol, atenolol, practolol, metoprolol, H 87/07 and tolamolol on bronchial or tracheal beta adrenergic receptors of both species were found. With respect to atrial beta adrenergic receptors, significantly lower pA2 values for human preparations, as compared to guinea-pig preparations, were found for tolamolol and CI 775. These are the only two agents in the series that derive their cardioselectivities from specific nitrogen substitutents. The different potencies of only these two compounds in antagonizing isoproterenol on atrial beta adrenergic receptors of both species suggest a difference in an accessory receptor area close to the site that interacts with the nitrogen atom of beta adrenergic agents.

Adrenergic beta-Antagonists↗
PubMed1976

The cardiovascular pharmacology and hemodynamic activity of tazolol, a selective myocardial beta-stimulant.

The pharmacology and hemodynamics of tazolol (1-iso-propylamino-3-(2-thiazoloxy)-2-propranolol HC1), a selective myocardial beta-stimulant, were studied in pentobarbital anesthetized dogs. Tazolol, i.v., increased myocardial contractile force and heart rate, but induced only minimal changes in arterial pressure. The cardiac effects of tazolol were blocked by pretreatment with the beta-blockers propranolol or practolol and inhibited in animals made tachyphylactic to amphetamine. They were not altered by pretreatment with hexamehtonium, atropine or reserpine. Tazolol increased left circumflex coronary artery flow to a far greater extent than a dose level of isoproterenol which produced a greater increase in cardiac output. Tazolol also increased superior mesenteric artery flow, whereas isoproterenol decreased it. Renal artery flow was not altered. Tazolol was also found to be orally active and to possess some mild general beta-blocking activity.

Adrenergic beta-Agonists↗
PubMed2001

[Enantiomeric separation of drugs based on macrocyclic antibiotics].

The present review paper describes the properties of the macrocyclic antibiotics vancomycin, teikoplanin, and ristocetin A, which can be used as stationary phases for separation of the enantiomers of drugs containing a stereogenic centre. It analyzes the results obtained in the separation of amino acids, its derivatives, loxiglumide, clenbuterol, practolol, carnitine, levodopa, methyldopa, ceftazidine, alkoxyphenylcarbamic acid derivatives, dichloroprop, ketoprofen, warfarin, and ergot alkaloids by means of high-performance liquid chromatography (HPLC).

Amino Acids↗
PubMed1987

ECT for Post-stroke Depression: Beta Blockade to Modify Rise in Blood Pressure.

A 60-year-old normotensive woman, who 3 years previously had had a cerebral haemorrhage, developed a severe depressive illness that failed to respond to tricyclic antidepressants and lithium, alone and combined. Electroconvulsive therapy (ECT) was administered using intravenous beta-blockade with practolol and atenolol prior to induction of anaesthesia to prevent the surge in blood pressure normally seen following the convulsion. The blood pressure did not rise and her depression responded to a series of nine ECT treatments. There were no associated complications.

Journal Article↗
PubMed1975

Method for the production of severe ventricular dysrhythmias in small laboratory animals.

In earlier reports from this laboratory, it was shown that 3 weeks' pretreatment with desoxycorticosterone acetate (DCA) pellet implantation and saline as drinking fluid caused a nearly 20,000-fold potentiation of the acute cardiotoxicity of isoproterenol. In such animals, the beta-receptor stimulant consistently elicited severe ventricular dysrhythmias, usually leading to ventricular fibrillation (VF) and death. In the present study, a similar enhancement of isoproterenol arrhythmogenic activity after DCA-saline pretreatment was demonstrated also in the guinea pig and albino mouse. It was found, further, that isoproterenol consistently caused an alteration of the total myocardial electrolyte content in DCA-saline-treated rats, consisting of a decrease of magnesium (Mg) and potassium (K) levels and elevation of sodium (Na). In control rats, on the other hand, isoproterenol did not alter the myocardial Mg content and increased K. The emertence of cardiac irregularities and VF could be inhibited by pretreatment with antiarrhythmic drugs. On a molar basis, these agents decreased the incidence of VF in the following descending order: dl-propranolol (100), practolol (39), d-propranolol (34), sotalol (20), quinidine (8), and lidocaine (5). In the presence of any of the listed drugs, except for lidocaine, isoproterenol did not lower Mg levels and had variable effects on those of Na and K. Pretreatment with Mg gluconate was likewise effective in preventing isoproterenol-induced dysrhythmias and death. These findings demonstrate that: a) sensitization of the myocardium by DCA-saline treatment is not species-specific for the rat; b) this phenomenon can be a useful method for the screening of antiarrhythmic drugs; and c) isoproterenol-induced dysrhythmias may be associated with myocardial electrolyte alterations involving especially Mg depletion.

Animals↗
PubMed1975

The effect of beta-phenylethylamine on temperature in mice and its possible mechanisms of action.

Beta-phenylethylamine on injection into mice (100 mg/kg i.p.) produces a marked hyperthermia which is followed by a prolonged hypothermia. The hyperthermic response was studied in this report. The hyperthermic response was inhibited by p-chlorophenylalanine, methysergide, cyproheptadine, alpha-methyl-tyrosine, propranolol, practolol, phenoxybenzamine, phentolamine, haloperidol, pimozide, protriptyline and desipramine. Lysergic acid diethylamide potentiated the response, while p-chloroamphetamine was without effect. While FLA-63 potentiated the response, disulfiram and reserpine were ineffective in preventing the hyperthermia. Nicotinic acid and prostaglandin E1 did not prevent PE induced hyperthermia. It was concluded from these results that PE induced hyperthermia in mice is blocked by agents that reduce the effective concentration of either DA or 5-HT in the central nervous system (by either synthesis inhibitors or receptor blockers). The involvement with catecholaminergic neurons at least was postulated to be a result of PE induced release of DA from DA neurons.

Animals↗
PubMed1976

Effect of PGA1, PGE2, diazoxide on myocardial contractile force.

Experiments were conducted in anesthetized dogs comparing the effects of PGA1, PGE2, and diazoxide on myocardial contractile force (MC). The three agents were given in successive bolus injections intravenously in equidepressor doses and myocardial contractile force was measured by means of a strain-gauge arch sutured onto the right ventricle. The drugs were administered before and during ganglionic (hexamethonium) and beta-blockade (practolol). Both PGA1, and PGE2 caused a marked rise in MC, 24 and 20 per cent, respectively, before blockade and 10 and 11 per cent during blockade. Diazoxide caused only a minimal rise, 0.9 per cent, before blockade and a marked fall, 27 per cent, during blockade. Diazoxide administration during left ventricular bypass indicates that the decrease in MC is not a direct result of alterations in preload or after load. It is suggested that hypertensive patients treated with autonomic blocking agents may be more susceptible to heart failure in response to diazoxide therapy.

Adrenergic beta-Antagonists↗
PubMed1977

Effect of beta-blocking agents and angiotensin II on isoproterenol-stimulated renin release from rat kidney slices.

UNLABELLED: Mechanisms by which beta-blocking agents decrease blood pressure and suppress renin release are incompletely understood. We previously demonstrated that renin release by kidney slices may be increased by beta-adrenergic agonists, and the present communication contains our results on the effects of 15 beta-blocking agents and angiotensin II on isoproterenol-stimulated renin release. None of the beta-blocking compounds inhibited basal renin release. Each agent was evaluated at concentrations ranging from 10-8 to 10-5 m and three different dose-response curve patterns were observed: (1) Metoprolol, acebutolol, labetalol, and d-propranolol had no effect on isoproterenol-stimulated renin release at any concentration, whereas pindolol and bufuralol demonstrated minimal inhibition at 10-5 m only. (2) Isoproterenol stimulation was completely inhibited when dl- or l-propranolol, alprenolol, and sotalol were administered at doses ranging between 5 x 10-6 and 10-6 m; but greater concentration of these agents resulted in reappearance of the isoproterenol response. (3) Dose-related inhibition was observed with practolol, oxprenolol, timolol, nadolol, and atenolol at concentrations ranging from 10-8 to 10-5 m. Basal renin release was significantly (P is less than 0.01) inhibited by angiotensin II at 10-6 m, which also inhibited isoproterenol-stimulated renin release in a dose-related fashion. [Sar1, Ala8] angiotensin II had no direct effects on either basal or isoproterenol-stimulated renin release, but blocked the inhibitory action of angiotensin II on these parameters. CONCLUSIONS: There are three different effects of beta-blocking agents on isoproterenol-stimulated renin release which can only partially be explained by their presently ascribed pharmacological properties. (Beta 1- and beta2-agonists, intrinsic sympathomimetic activity, membrane-stabilizing actions). Angiotensin II inhibition of renin release appears to be functionally related to adrenergic pathways.

Adrenergic beta-Antagonists↗
PubMed1977

[Quantitative parameters of sympatho-neuronal and sympatho-adrenal activities in man. The influence of beta-receptor blocking agents (author's transl)].

Determination of both catecholamine concentrations (norepinephrine and epinephrine) and the activity of dopamine-beta-hydroxylase in the plasma of health volunteers and hypertensive patients leads to the conclusion that these parameters used together can be considered an index for sympathetic neuronal activity. However, highly specific and sensitive radiometric methods are necessary for the measurement of these biochemical parameters. In healthy volunteers and hypertensive patients after acute and chronic administration of beta-adrenergic blocking agents, e.g., propranolol, practolol or penbutolol, a significantly higher increase of catecholamine concentrations in the plasma has been observed during physical exercise. This pronounced increase in plasma catecholamine concentrations (mainly norepinephrine) is probably due to an enhanced compensatory sympathetic neuronal activity, accompanied by an increased peripheral resistance; this is obviously necessary in order to maintain a sufficient perfusion of peripheral tissues during work load under the influence of beta-adrenergic blocking agents, since an adequate cardiac output is prohibited by blockade of adrenergic beta-receptors. On the other hand, the pronounced increase in sympathetic tone after beta-blockade, especially after administration of high doses, could be responsible for certain reported side effects, such as hypertensive crisis in psychiatric patients or in patients with phaeochromocytoma.

Adrenal Medulla↗
PubMed1975

Opposing regulatory influences of cyclic guanosine monophosphate and cyclic adenosine monophosphate in the control of cardiac muscle contraction.

The effects of acetylcholine chloride (ACh) and isoproterenol (Iso) on myocardial levels of guanosine 3', 5'-monophosphate (cyclic GMP) and adenosine 3', 5'-monophosphate (cyclic AMP) and on force of contraction were studied in elelctrically driven isolated rabbit atria. Incubation of atria with Tyrode's solution containing ACh (5 x 10(-7) M) produced significant decreases in contractile force that were associated with significant elevations in atrial cyclic GMP levels. Atrial levels of cyclic AMP were significantly lowered at 15 sec after the addition of ACh but were only slightly lowered at earlier time intervals. The effects of acetylcholine on force of contraction and on cyclic nucleotide levels were prevented with atropine (1 x 10(-7) M). The addition of Iso (1 x 10(-7)-M) to isolated atria produced significant increases in contractile force that were associated with significant elevations in effects of Iso on force of contraction and on cyclic nucleotide levels were prevented with practolol (1 x 10(-5) M). The increases in atrial cyclic GMP and cyclic AMP levels following addition of ACh and Iso, respectively, precede the changes in contractile force. These data support our hypothesis that cyclic AMP and cyclic GMP exert oppositional effects on cardiac contrctility.

Acetylcholine↗
PubMed1975

Oppositional effects of acetylcholine and isoproterenol on isometric tension and cyclic nucleotide concentrations in rabbit atria.

The effects of acetylcholine chloride and isoproterenol on myocardiial cyclic GMP, cyclic AMP and on isometric tension were studied in isolated electrically driven rabbit atria. Acetylcholine (0.5 muM) produced a significant decrease in isometric force that was associated with a significant elevation in atrial cyclic GMP. Cyclic AMP was significantly lowered at 15 seconds after the addition of acetylcholine, but was only slightly decreased at earlier time periods. Both the negative inotropic action and increase in cyclic GMP after addition of acetylcholine were blocked by atropine. Isoproterenol (0.1 muM) produced a significant increase in isometric tension that was associated with a significant elevation in atrial cyclic AMP levels, whereas cyclic GMP levels were not changed. These effects were blocked by practolol. The increases in atrial cyclic GMP and cyclic AMP following addition of acetylcholine and isoproterenol, respectively, preceded the changes in isometric tension in response to these agents. These data support the hypothesis that changes in intracellular levels of cyclic AMP and cyclic GMP may mediate the positive and negative inotropic effects of adrenergic and cholinergic agents.

Acetylcholine↗
PubMed1977

Cardiac action of carazolol and methypranol in comparison with other beta-receptor blockers.

The new beta-blockers 4-(2-hydroxy-3-isopropyl-amino-propoxy)-carbazole (carazolol) and 1-(4-acetoxy-2,3,5-trimethylphenyloxy)-3-isopropylamino-propan-2-ol (methypranol, Disorat) were compared with 14 well-known beta-blocking agents with regard to isoproterenol antagonism (equipotent doses in the rabbit i.v.), acute toxicity (LD50 in mice i.v.) and intrinsic sympathomimetic activity (increase in the heart rate of reserpinized rats i.p.). The following descending order for the equipotent beta-receptor blocking doses was obtained: nifenalol, DCI, pronethalol, practolol, sotalol, alprenolol, bupranolol, toliprolol, propranolol, methypranol, YB 2 pindolol, bunitrolol, oxprenolol, bunolol and carazolol. Carazolol had, in addition, the highest therapeutic index and at beta-receptor blocking doses virtually no intrinsic sympathomimetic activity.

Adrenergic beta-Antagonists↗
PubMed1991

Mechanism of inotropic action of xestoquinone, a novel cardiotonic agent isolated from a sea sponge.

Xestoquinone (XQN) isolated from the sea sponge Xestospongia sapra produced dose-dependent cardiotonic effects on guinea pig left and right atria. A direct action of XQN (1-30 microM) on the contractile machinery of cardiac myofilaments was demonstrated in chemically skinned fiber preparations from guinea pig papillary muscles. In atrial preparations, the XQN-induced inotropic effect was markedly inhibited by verapamil or nifedipine, but was not affected by practolol, chlorpheniramine, cimetidine, tetrodotoxin or reserpine. The Ca++ dependence curve for the contractile response of the atria was substantially shifted to the left by XQN (10 microM), and this XQN-induced shift was reversed by verapamil. The time-to-peak tension and relaxation times of the atrial contractions were shortened by XQN, and the action potential duration was markedly prolonged. Whole-cell patch clamp recordings in left atrial strips confirmed that XQN (30 microM) increased the slow inward current. However, there was a temporal dissociation between altered tension development and prolongation of the action potential duration. Cyclic AMP phosphodiesterase activity was inhibited and tissue cyclic AMP content of guinea pig left atria was increased by XQN (0.3-10 microM) in a concentration-dependent manner, but increases in cyclic AMP content did not occur in parallel with increases in contractile response. These observations suggest that an enhancement of intracellular cyclic AMP content and Ca++ influx across the cell membrane contribute to the late phase of XQN-caused cardiotonic responses, whereas the early phase may largely be elicited through direct activation of contractile elements. XQN may provide a novel leading compound for valuable cardiotonic agents.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1977

The beta-adrenoceptors responsible for a direct relaxation of the uncontracted nictitating membrane of the anaesthetized cat.

Direct relaxation of the nictitating membrane of the anaesthetized cat was produced by close intra-arterial injections of single doses of isoprenaline and other beta-adrenoceptor agonists. This response was relatively resistant to blockade by doses of propranolol that almost abolished the corresponding positive chronotropic and vasodepressor responses. Construction of dose-response curves, however, revealed antagonism of all three parameters by propranolol and different sensitivities of the parameters to isoprenaline. The absence of blockade by practolol, although negative evidence, permitted the nictitating membrane response to be classified as a beta2-adrenoceptor effect, which was supported by the full agonist activity of salbutamol. The blockade of the nictitating membrane response by propranolol was however weaker than of the beta2-adrenoceptor mediated vasodepressor response. Contractile responses were observed with higher doses of isoprenaline and after intravenous injection. These were probably indirect effects induced by local changes in blood pressure at the nictitating membrane due to the concommitant vasodepressor response.

Albuterol↗