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PubMed1989

The adrenocorticotropic hormone (ACTH)-induced reversal of hemorrhagic shock.

Adrenocorticotropic hormone (ACTH), while having negligible effects on cardiovascular function in the intact animal, induces a potent and sustained reversal of an otherwise invariably, rapidly fatal condition of hemorrhage-induced hypovolemic shock, in rats and dogs. The main site(s) of action are at the peripheral level; however, subsidiary site(s) of action in the CNS cannot be excluded. The studies on the mechanism of action indicate that the ACTH-induced reversal of hemorrhagic shock (a) is an extra-hormonal, adrenal-independent effect, because it is not affected by adrenalectomy and is shared by many ACTH-fragments practically devoid of corticotropic activity; (b) is antagonized by morphine in a surmontable way; (c) needs the functional integrity of the sympathetic nervous system (it is prevented by guanethidine, reserpine, and clonidine) and the availability of peripheral alpha-adrenoceptors (it is antagonized by dibenamine, prazosin and yohimbine, but not by practolol); (d) requires the integrity of afferent vagal fibers (it is almost completely abolished by vagotomy); (e) involves central cholinergic networks (it is antagonized by atropine sulphate, but not by atropine methyl bromide; and it is prevented by the intracerebroventricular injection of hemicholinium-3); (f) is associated with a massive increase in the volume of circulating blood, likely due to a mobilization from peripheral pooling sites (it is largely prevented by splenectomy or by suprahepatic veins ligature, and is associated with a restoration of the venous blood flow in peripheral vascular beds and with a normalization of venous PO2); (g) is associated with a restoration of heart and spleen adrenoceptors, whose number is significantly decreased during hemorrhagic shock. The survival time of hemorrhage-shocked animals, which is 26 +/- 3 min in controls, is greatly prolonged (44 +/- 18 h) by ACTH, provided that the treatment is made within 5-10 min after bleeding. Finally, in animals treated with ACTH within 5-10 min after bleeding, blood reinfusion retains its effectiveness and reverse shock even if performed 2-5 h later.

Adrenocorticotropic Hormone↗

PubMed1988

Autoradiographic localization of beta-adrenergic receptors in rat oviduct.

Catecholamines are known to have an inhibitory effect on oviductal smooth musculature by changing the adrenergic receptors activity. In order to further investigate the role of epinephrine and/or norepinephrine in oviduct, the distribution of beta-adrenergic receptors has been studied in the rat oviduct, using in vitro autoradiography and [125I]cyanopindolol (CYP), as radioligand. The specificity of the labelling and the characterization of receptor subtypes in different cell types was achieved by displacement of radioligand with increasing concentrations of zinterol, a beta-adrenergic agonist with preferential affinity for the beta 2-adrenoreceptor subtype and practolol, a beta-adrenergic antagonist that binds preferentially to beta 1-subtype. Quantitative estimation of ligand binding was achieved by densitometry. It was shown that the vast majority of beta-receptors were of the beta 2-subtype and were found in smooth muscle layers as well as in the epithelium. The latter localization suggests a role for epinephrine and/or norepinephrine on the oviductal epithelium.

Animals↗

PubMed1976

The effect of beta-adrenergic blocking agents on experimental porphyria induced by 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) in vivo and in vitro.

The effect of DL-propranolol on 3',5'-diethoxycarbonyl-1,4-dihydrocollidine-induced experimental porphyria was studied. DL-Propranolol, a beta-adrenergic blocking agent with non-specific membrane effects, partially inhibited 3',5'-diethoxycarbonyl-1,4-dihydrocollidine-induced delta-aminolevulinate synthetase activity both in rats and in chick embryo liver cells in culture. In rats, DL-propranolol decreased urinary delta-aminolevulinate and porphobilinogen but no change occurred in the 24-h urinary excretion of total porphyrins and in the concentration of porphyrins in the liver. In cultured chick embryo liver cells treated with 3',5'-diethoxycarbonyl-1,4-dihydrocollidine, DL-propranolol decreased accumulation of porphyrins in the medium. D-Propranolol, oxprenolol and quinidine acted like DL-propranolol in chick embryo liver cells in culture treated with 3',5'-diethoxycarbonyl-1,4-dihydrocollidine. Pindolol, practolol and lidocaine had no effect. Phenobarbitone had a synergistic effect on the induction of delta-aminolevulinate synthetase by 3',5'-diethoxycarbonyl-1,4-dihydrocollidine in cultures of chick embryo liver cells. This induction was partially inhibited by propranolol. However, the increased accumulation of porphyrins in the medium caused by 3',5'-diethoxycarbonyl-1,4-dihydrocollidine was inhibited by the addition of phenobarbitone. This inhibited induction was further decreased by propranolol. Most of our results indicate that the drugs tested act mainly by their effects on membranes.

5-Aminolevulinate Synthetase↗

PubMed1983

Characterization of beta-adrenergic receptor subtypes in androgen-induced mouse kidney hypertrophy using a new high-affinity ligand, [125I]iodocyanopindolol.

In fully developed androgen-induced hypertrophy of female mouse kidney, beta-adrenergic receptors per unit membrane protein were increased approx. 2.5-fold, as measured by the binding of [125I]iodocyanopindolol, with no change in apparent dissociation constants (Kd range 20-25 pM). Membrane protein relative to total kidney protein, Na+/K+-dependent ATPase (EC 3.6.1.3) and 5'-nucleotidase (EC 3.1.3.5) activities and cholesterol content per unit membrane protein did not differ significantly in preparations from control and treated animals. The binding of iodocyanopindolol to kidney membranes was characterized with respect to association and dissociation kinetics, and also in regard to the less-specific contributions of other major catecholamine or indolamine receptors, using mixtures of the corresponding specific competitors. beta 1-selective drugs, practolol and metoprolol, and beta 2-selective agents, IPS-339 and zinterol, were competed with iodocyanopindolol to assess the receptor type specificity, and the ensuing binding profiles were dissected by a nonlinear regression analysis as described by Munson, P.J. and Rodbard, D. (Anal. Biochem. (1982) 107, 220-239). Most of the androgen-induced beta-adrenergic receptors had the binding properties corresponding to beta 2-subtype. No consistent increase in the density of beta 1-adrenergic receptors could be shown.

Androgens↗

PubMed1983

Mechanism of action of phenylephrine on isolated guinea-pig atria rate.

1. Phenylephrine has a positive chronotropic effect on the right isolated guinea-pig atria and this effect is not modified by alpha-adrenergic blocker (phentolamine) but it is drastically inhibited by beta-adrenergic antagonists (practolol or propranolol). 2. The effect is substantially reduced by treatment with cocaine or pretreatment with reserpine. 3. Cocaine plus reserpine shift the dose-response curve for phenylephrine to the left. 4. It is concluded that positive chronotropic effect of phenylephrine has two components: direct action on beta-adrenergic receptors and an indirect action due to norepinephrine release.

Adrenergic alpha-Antagonists↗

PubMed1987

Partial agonists at guinea-pig atrial beta-adrenoceptors display relaxation responses in the guinea-pig ileum independent of beta-adrenoceptor stimulation.

The beta-adrenoceptor mediated responses of oxyfedrine, ritodrine, tazolol, prenalterol, salbutamol and carteolol were examined on guinea-pig left and right atrial and ileal preparations. All agonists tested in left and right atrial preparations were partial agonists relative to isoprenaline. All agonists with the exception of salbutamol, which appeared a full agonist, produced relaxation responses significantly greater than isoprenaline in ileal preparations. The response to ritodrine in the ileum was not influenced by practolol, in a concentration which antagonized the responses of ritodrine in the right atria. The response of the ileum to beta-adrenoceptor antagonists of varying lipophyllicity was examined. Propranolol and pindolol both produced relaxation responses relative to their lipophyllicities. No relaxation was observed to atenolol, which exhibits very low lipophyllicity. It is concluded that beta-adrenoceptor agonists exhibit a substantial relaxation of guinea-pig ileum that is independent of beta-adrenoceptor stimulation.

Adrenergic beta-Agonists↗

PubMed1991

Adrenalin activation of beta 2-adrenoceptors stimulates morphological changes in astrocytes (pituicytes) cultured from adult rat neurohypophyses.

Neurohypophysial astrocytes, the pituicytes, are known to undergo morphological changes in vivo in response to stimuli that increase the demand for hormone secretion. Similar changes have been induced by beta-adrenergic stimulation both in the isolated, but otherwise intact, neural lobe and in pituicytes cultured from adult rats. Since the predominant beta-receptor subtype in the neural lobe is beta 2, we investigated the possibility that beta 2-receptor activation is mainly responsible for the observed pituicyte responses. In one experiment, cultured pituicytes were induced by noradrenalin to change from flattened amorphous to stellate morphology. Addition of the beta 2-antagonist IPS 339, but not the beta 1-antagonist practolol, significantly reduced (by 30-60%) the number of cells transformed by noradrenalin. In a second experiment, adrenalin, by definition a more potent beta 2-agonist, transformed significantly more pituicytes into stellate shapes than did noradrenalin at the same concentrations (100% vs. 60% increase, respectively). These results support the idea that beta 2-adrenergic receptors are involved in neurohypophysial plasticity. Also, since the neural lobe is outside of the bloodbrain barrier, these findings suggest that adrenal catecholamines participate in altering pituicyte morphology.

Adrenergic beta-Agonists↗

PubMed1983

Effect of some beta-adrenergic blocking agents on tissue guanylate cyclase and cyclic nucleotides in the rat.

Pretreatment of rats with the beta-adrenergic blocking agents, atenolol, practolol, pronethalol and propranolol, at a dosage of 150 mg/kg/day for 5 days, produced marked increases in guanylate cyclase activity in the liver, gastric and intestinal mucosae, but with concomitant decreases in cyclic GMP levels. The ratios of cAMP/cGMP in each of the tissues were not changed significantly from control values after pretreatment with these drugs. These observations indicate that any oncogenicity seen with beta-blocking agents is not due to the common pharmacological action of beta-adrenoreceptor blockade.

Adrenergic beta-Antagonists↗

PubMed1991

Reversed-phase high-performance liquid chromatographic analysis of atenolol enantiomers in plasma after chiral derivatization with (+)-1-(9-fluorenyl)ethyl chloroformate.

A sensitive high-performance liquid chromatographic method for the determination of the enantiomers of atenolol in rat plasma has been developed. Racemic atenolol and practolol (internal standard) were extracted from alkalinized plasma (pH 12) into dichloromethane containing 3% (v/v) heptafluoro-1-butanol, and the organic layer was evaporated. The samples were derivatized with (+)-1-(9-fluorenyl)ethyl chloroformate at pH 8.5 for 30 min. After removal of excess reagent, the diastereomers were extracted into dichloromethane. The diastereomers were separated on a Microspher C18 column (3 microns) with a mobile phase of acetonitrile-sodium acetate buffer (0.01 M, pH 7) (50:50, v/v) at a flow-rate of 0.8 ml/min. Fluorescence detection (lambda ex = 227 nm, lambda em = 310 nm) was used. When 100 microliters of plasma were used, the quantitation limit was 10 ng/ml for the atenolol enantiomers. The assay was applied to measure concentrations of atenolol enantiomers in plasma after intravenous administration of racemic atenolol to rats.

Animals↗

PubMed1994

Determination of dapsone in serum and saliva using reversed-phase high-performance liquid chromatography with ultraviolet or electrochemical detection.

A simple, extractionless method for the determination of dapsone in serum and saliva is described. Reversed-phase high-performance liquid chromatography is used with UV detection at 295 nm or electrochemical detection at 0.7 V. Diazoxide in buffer is the internal standard for UV detection and practolol for electrochemical detection. Sample preparation is minimal with protein precipitation of serum samples whilst saliva samples are simply diluted with addition of an internal standard. Low-level serum and saliva samples are front-cut on-line with a 3 cm laboratory-made precolumn in the loop position on a standard Valco injection valve. Isocratic separation is achieved on a 250 mm x 4.6 mm I.D. stainless-steel Spherisorb S5 ODS-1 column. The mobile phase for high levels of dapsone is acetonitrile-elution buffer (12:88, v/v) at 2 ml/min and a column temperature of 40 degrees C for both serum and saliva separations. For the low-level assays using electrochemical detection and solid-phase clean-up, the mobile phase is acetonitrile-methanol-elution buffer (9:4:87, v/v/v). The UV and electrochemical detection limits are 25 ng/ml and 200 pg/ml, respectively, in both serum and saliva. This simple method is applicable to the routine monitoring of dapsone levels in serum from leprotic patients and electrochemical detection gives a simple, reliable method for the monitoring of trough values in subjects on anti-malarial prophylaxis.

Chromatography, High Pressure Liquid↗

PubMed1989

A strategy for the determination of beta blockers in plasma using solid-phase extraction in combination with high-performance liquid chromatography.

This paper describes a general approach for the therapeutic drug monitoring of 13 different beta blockers in plasma. The chromatographic system contains a cyanopropyl-bonded phase as a stationary phase in combination with a mobile phase composed of acetonitrile and phosphate buffer (pH = 3, mu = 0.05). Two modes of detection are used, namely, UV detection and fluorescence detection. The sample pretreatment is performed with a nitrile-sorbent in combination with methanol-phosphate buffer (pH = 3, mu = 0.05) or with methanol containing 0.1% propylamine as eluent. Acceptable recoveries are obtained for practolol, acebutolol, pindolol, oxprenolol, mepindolol, atenolol, propranolol, prenalterol, alprenolol, metoprolol, sotalol and nadolol. For labetalol, however, the elution recovery has to be improved. Finally, this approach is illustrated by the assay of nadolol in the plasma of patients suffering from hypertension, who had received an oral formulation of the drug.

Adrenergic beta-Antagonists↗

PubMed1984

Specificity of beta-adrenergic control of lipolysis in swine adipose tissue.

Fenoterol (beta 2-agonist) and several analogs stimulated swine adipose tissue lipolysis in addition to epinephrine, norepinephrine and isoproterenol. Lipolytic activity was inhibited by propranolol (beta 1 + beta 2) greater than metoprolol (beta 1) greater than ICI 118,551 (beta 2) greater than practolol (beta 1) much greater than butoxamine (beta 2) regardless of the agonist used in the test system. The swine adipose adrenoceptor is not readily classified into a beta 1 or beta 2 subtype. It may be unique or the classification systems devised in laboratory animals may not be applicable across species.

Adipose Tissue↗

PubMed1986

Are beta-adrenergic receptors in ventricular muscles of carp heart (Cyprinus carpio) mostly the beta-2 type?

The positive inotropic effect of isoproterenol was quantified in the presence of several beta-adrenergic blocking agents in ventricular strips of carp heart. Isoproterenol had a concentration-dependent positive inotropic effect. The effect was markedly inhibited by propranolol and carteolol, but was extremely insensitive to atenolol. Practolol totally failed to alter the effect. These results indicated that the positive inotropic effect of isoproterenol may be mediated by mostly beta-2 adrenergic receptors in ventricular strips of carp heart.

Adrenergic beta-Antagonists↗

PubMed2001

Quantitative structure-retention and retention-activity relationships of beta-blocking agents by micellar liquid chromatography.

Sixteen beta-blocking agents (acebutolol, alprenolol, atenolol, bisoprolol, carteolol, celiprolol, esmolol, labetalol, metoprolol, nadolol, oxprenolol, pindolol, practolol, propranolol, sotalol and timolol) showing a large range of hydrophobicity (octanol-water partition coefficients, log P between -0.026 and 2.81) were subjected to micellar liquid chromatography with sodium dodecyl sulfate as micelle forming agent, and n-propanol as organic modifier. The correlation between log P and the retention factor extrapolated to a mobile phase free of micelles and organic modifier was investigated. The use of an interpolated retention factor or the retention factor for specific individual experimental mobile phases was however advantageous since the retention factors of all beta-blocking agents were measurable in the selected mobile phases. Good correlations with log P and with in vitro biological parameters (cellular permeability coefficients in Caco-2 monolayers and apparent permeability coefficients in rat intestinal segments) were found.

Adrenergic beta-Antagonists↗

PubMed1985

Myocardial injury following endogenous catecholamine release in rabbits.

Catecholamines (CAT) given in large doses produce cardiomyopathic changes in several animal species. This study was designed to determine if endogenous release can also induce cardiac injury. Rabbits were infused with doses of tyramine (TYR), ranging from 200 to 500 micrograms/min/kg, i.v. for 90 min. Arterial pressure and heart rate were measured, as were total CAT concentrations, blood gases, pH and glucose. Two days later the animals were killed and cardiac injury assessed using a histological scoring system. All data were compared with controls given saline. Initial CAT averaged 452 pg/ml, rose to 2890 pg/ml after starting TYR, 500 micrograms/min/kg, and remained elevated for the duration of infusion. Circulating CAT levels were a function of TYR dose, and bore a linear relationship to the histological score (P less than 0.001). Development of lesions was unaltered by beta 1 blockade with practolol, but sharply reduced by alpha blockade with phentolamine (P less than 0.01). Pretreatment with insulin also reduced lesion formation, but diabetic (alloxan) rabbits showed no greater CAT injury. It is concluded that endogenous release of CAT induces myocardial injury in the rabbit in a dose-dependent manner. This is unrelated to myocardial O2 demand, and microvascular pathology was absent. Activation of alpha adrenergic pathways is likely the dominant or exclusive mechanism.

Animals↗

PubMed1988

Isolation of basic drugs from plasma using solid-phase extraction with a cyanopropyl-bonded phase.

The use of a CN sorbent for the isolation of basic compounds from plasma is described. Adsorption from water and plasma was investigated for a test set of 30 basic drugs. It was found that compounds with a carbon chain length greater than or equal to 11 are totally retained and that the competitive effect of the matrix on the adsorption is minimal. Methanol-phosphate buffer (pH 3, mu = 0.05) (50:50) yielded good recoveries for more polar compounds; apolar basic drugs can be efficiently eluted using methanol containing 0.1% propylamine. Water up to 3 ml can be used for the washing step. This approach was applied to the determination of eight drugs in plasma at therapeutic levels. The absolute recoveries (n = 6) obtained were 98.8 +/- 7.3% for papaverine, 82.3 +/- 3.9% for practolol, 83.4 +/- 2.6% for metoclopramide, 87.3 +/- 5.8% for imipramine, 82.8 +/- 3.3% for procaine, 82.7 +/- 4.6% for morphine, 87.5 +/- 7.2% for propranolol and 90.4 +/- 6.2% for yohimbine.

Adsorption↗

PubMed1989

Beta 2-adrenoceptor stimulation inhibits ganglionic transmission in ferret trachea.

To study the effect of beta-adrenoceptor stimulation on the transmission through airway parasympathetic ganglia, we used an in vitro nerve-muscle preparation of ferret trachea. Isometric muscle contractions were induced for 20 s every 2 min alternating with postganglionic activation by electrical field stimulation (EFS) or with preganglionic activation by direct nerve stimulation (DNS). The pulse frequency was always 12 Hz. A possible modulation of ganglionic transmission was assessed by comparing contractions induced by DNS to contractions induced by EFS. In 9 experiments isoprenaline initially reduced the response to EFS and DNS to the same extent, indicating an effect on postganglionic structures. After 20-30 min exposure the response to preganglionic activation by DNS was further reduced indicating an inhibition of ganglionic transmission. The concentration/response relationship for the ganglionic effect of isoprenaline was shifted about ten times to the right by 0.1 microM propranolol (n = 5) and by a beta 2-adrenoceptor-antagonist (0.1 microM ICI 118.551) (n = 8), whereas a beta 1-adrenoceptor-antagonist (10 microM practolol) had no, or only slight, effect. In two experiments pretreatment by 0.1 microM phenoxybenzamine for 20 min did not prevent ganglionic inhibition by 0.3 microM isoprenaline. We conclude that parasympathetic ganglia in ferret trachea have beta-adrenoceptors mediating inhibition of ganglionic transmission, and that these probably are of the beta 2 type. Tentatively these receptors could be operated upon by circulating catecholamines.

Adrenergic beta-Agonists↗

PubMed1981

2-Benzodioxinylaminoethanols: a new class of beta-adrenergic blocking and antihypertensive agents.

Various 2-benzodioxinylaminoethanol derivatives were synthetized and investigated for beta-adrenergic blocking activity. Most compounds demonstrated a beta-blocking activity of a competitive type when evaluated in guinea pig atrial and tracheal preparations. Three compounds were more potent than practolol and propranolol. All compounds demonstrated antihypertensive properties in spontaneously hypertensive rats. The most active compound was 1-(1,4-benzodioxin-2-yl)-2-[N4-(2-methoxyphenyl)piperazino]ethanol (11), which at 2.5 mg/kg iv lowered blood pressure by 41%.

Adrenergic beta-Antagonists↗