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At least 307 records · Page 17Linked to original sources
PubMedDate not supplied

[Age-related characteristics of the effect of adrenomimetics and adrenoblockaders on the calcium and magnesium content of the rat myocardium].

The effects of noradrenaline (0.025 mg/kg), izadrin (0.1 mg/kg), adrenaline (0.025 mg/kg), ephedrine (5 mg/kg) phentolamine (5 mg/kg), dibenamine (5 mg/kg), anaprilin (1 mg/kg), alpheprol (1 mg/kg) on calcium and magnesium contents in the myocardium of growing rats (7 and 30 days, 3-5 months) were studied. During the animal development and growth the effects of adrenomimetics on calcium and magnesium metabolism decrease to a lesser degree than those of adrenoblockers. The data obtained indicate the enhancement of the regulatory factors and attenuation of the metabolic factors of the mechanism of adrenergic agents' action in the process of the postnatal development.

Aging↗
PubMed1986

Prazosin selectively antagonizes norepinephrine contractions at low-affinity, non-alpha adrenoceptor sites (extraceptors) in arterial muscle.

The characteristics of a low-affinity site activated by norepinephrine (NE), which is demonstrable in arterial smooth muscle pretreated with phenoxybenzamine (PBZ) to alkylate most alpha adrenoceptors were studied. Treatment with PBZ resulted in biphasic dose-response curves to NE. The initial phase associated with concentrations of NE up to 10(-5) M was due to its action in tissues where alpha adrenoceptors have been reduced to a number that would not support a maximum contraction. The second phase occurred with higher doses of NE. We postulate that this latter PBZ-resistant phase or contraction, which can represent more than 60% of the control maximal response, occurs at low-affinity sites for NE "extraceptors" distinct from alpha adrenoceptors in arterial smooth muscle. These residual responses to NE after PBZ treatment were inhibited selectively by prazosin and protected by prazosin from further inhibition by additional doses of PBZ. Effects due to prazosin at low-affinity sites were observed only with doses in excess of those required to competitively inhibit responses through alpha adrenoceptors in smooth muscle. The response to NE occurring through PBZ-resistant adrenoceptors was not dependent on the presence of the endothelium. This low-affinity site for NE was also evident after alkylation of alpha adrenoceptors with other irreversibly acting antagonists (e.g., benextramine and dibenamine). These observations are discussed in relation to the suggestion for a new adrenoceptor, the gamma-adrenoceptor. Differences and similarities of the extraceptor with this proposed adrenoceptor are discussed. Both sites have a high threshold to NE, and both may be influenced by prazosin.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMedDate not supplied

[Effect of butyrophenone derivatives on D-serotonin reactive structures].

Droperidol, haloperidol and azabutyron inhibit the reactions of rabbit aortal stria caused by stimulation of D-type serotonine receptors. Droperidol appears most active in this respect. Its antiserotonine properties are characterised by certain selectivity. The capacity of droperidol for protection of D-receptors against irreversible dibenamine blockade suggests its indirect interaction with D-receptors.

Animals↗
PubMed1985

Do D 600 and diltiazem interact with serotonin receptors in rabbit vascular tissues?

This study investigates the interactive effects of Ca antagonists and responses to serotonin (5-HT) in isolated rabbit aorta and basilar artery. Isolated strips of rabbit aorta and of basilar artery were studied in organ baths containing 20 ml of Krebs-buffer solution. D 600 or diltiazem caused parallel rightward shifts of concentration-response curves for 5-HT in isolated rabbit aorta, but each reduced the 5-HT-induced maximum response in basilar artery. The slope values from Schild plot analyses in aorta were 1.11 +/- 0.05 and 1.22 +/- 0.37 in D 600 and diltiazem, respectively. Dibenamine pretreatment caused reduction of maximum response to 5-HT in both tissues. Such reduction was diminished markedly by the presence of D 600, diltiazem or 5-HT in aorta but not in basilar artery. Also, the antagonistic effects of D 600 and diltiazem were diminished by elevation of bath Ca in basilar artery but not in aorta. These results strongly suggest that the two Ca entry blockers used in this study might compete with 5-HT at 5-HT receptors in rabbit aorta and that the pharmacomechanical property of 5-HT receptors in rabbit aorta might be distinct from that in rabbit basilar artery.

Animals↗
PubMed1970

Temperature modulation of alpha- and beta-adrenoceptors in the isolated frog heart.

1. The effects of adrenaline on the isolated frog's heart at 27 degrees C are not antagonized by phentolamine (1.5 x 10(-6)M) but are abolished at 7 degrees C.2. At 27 degrees C isoprenaline was more potent than noradrenaline, but at 7 degrees C noradrenaline was more potent than isoprenaline.3. Phenoxybenzamine (1.5 x 10(-5)M) or dibenamine (1.5 x 10(-5)M) at 7 degrees C abolished the work output induced by adrenaline. When the temperature was raised to 24 degrees C, adrenaline caused an increase in work output.4. It is concluded that in the isolated frog heart there are at least two pools of adrenoceptors, the availability of which can be governed by temperature.

Animals↗
PubMed1981

Pharmacological responses by different portions of guinea pig vas deferens circular muscle preparation.

The different segments of the guinea pig vas deferens circular muscle exhibit differential response patterns upon pharmacological stimulation. Namely, apart from barium chloride, the affinity and intrinsic activity of certain agonists and the strength of maximum contractions they induce appear to decrease along the path from the epididymis toward the prostate. If one subdivides the vas deferens into 3 parts of equal length such as epididymal, medial and prostatic portions, then adrenaline, acetylcholine, acetyl-beta-methylcholine, dopamine, histamine and bradykinin induce contractions on each of the 3 parts; whereas tyramine, ephedrine elicit responses in the epididymal and medial portions; amphetamine, DMPP, serotonin and PGF2 alpha in turn provoking contractions exclusively on the epididymal portion. The effects of adrenaline and noradrenaline are blocked by phentolamine and tolazoline; the responses to acetylcholine, acetyl-beta-methylcholine and carbamyl-beta-methylcholine are antagonized by atropine over a specific concentration range. The effects of tyramine, ephedrine and amphetamine are inhibited by phentolamine in an remarkably low dose range (pA2 = 13.51 +/- 0.09; 14.54 +/- 0.31; 14.35 +/- 0.12). The situation was the same when tyramine-dibenamine and tyramine-phenoxybenzamine combinations were tested (pD'2 = 14.03 +/- 0.37; 13.26 +/- 0.03). Based on these findings the presence of a peculiar alpha adrenergic receptor is suggested on the sympathetic postganglionic fibres. In addition to the already identified alpha adrenergic, muscarinic cholinergic and histamine H1 receptors, we could show the presence of dopaminergic receptors too in the vas deferens circular muscle.

Acetylcholine↗
PubMed1982

[Relationship between arsenic-induced hypothermia and brain monoamines. (2). The roles of noradrenaline and dopamine].

It has been reported that hypothermia induced by intravenous administration of As2O3 3 mg/kg in rabbits is due to a decrease of noradrenaline (NA) in the hypothalamus. In this paper, the role of NA or dopamine (DA) on As2O3-induced hypothermia in rabbits were investigated. As2O3-induced hypothermia was not inhibited by pretreatment with FLA-63, a potent dopamine-beta-hydroxylase inhibitor, which produces an increase of DA and a decrease of NA in rabbit brain; and it was also inhibited by pretreatment with haloperidol or pimozide, potent DA-receptor blocking agents. On the contrary, pretreatment with phenoxybenzamine or dibenamine, alpha-receptor blocking agents, completely inhibited these hypothermia. These findings indicated that NA took an important part in thermoregulation in rabbits and certified that DA or DA-receptors were not involved As2O3-induced hypothermia.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

[Catecholamine content in the myocardium of growing rats with alpha- and beta-adrenergic blockades].

Studies of the effect of a single intraperitoneal injection of the alpha-adrenoblockers, phentolamine and dibenamine (5 mg/kg) and the beta-adrenoblockers, anapriline and alpheprol (1 mg/kg) into rats aged 7, 30 days and 3-5 months have demonstrated that as regards the degree of the changes in noradrenaline and adrenaline levels, the 7-day-old animals are more susceptible to the alpha-adrenoblockers, while the 30-day-old ones to the drugs of both groups. A relationship has been noticed between the age, the grade of the development of the adrenergic apparatus of the heart, metabolism of this organ and the pharmacodynamics of the adrenoblockers.

Adrenergic alpha-Antagonists↗
PubMed1984

Differential effects of the calcium entry blocker D 600 on contractions of rat and guinea-pig aortas, elicited by various alpha-1 adrenoceptor agonists.

Contractions of rat and guinea-pig aortas to the alpha-adrenoceptor agonists I-norepinephrine, cirazoline , St 587, clonidine and Sgd 101/75 and the effect of calcium entry blockade by D 600 on the responses were evaluated. In rat aorta, D-600 (10(-8) to 10(-5) M) effectively and concentration-dependently reduced the maximal responses to St 587, clonidine and Sgd 101/75 (maximal percentage inhibition 84 +/- 2.1, 86 +/- 4.1 and 65 +/- 2.8, n = 5-6, respectively) in contrast to those of I-norepinephrine and cirazoline (maximal percentage inhibition 23 +/- 2.1 and 21 +/- 4.1, n = 6, respectively). Reducing the receptor number on rat aorta by approximately 85% by means of the irreversible blocker dibenamine did not result in a greater sensitivity of norepinephrine-induced contractions toward D 600. Prazosin was found 800 to 1000 times more potent than yohimbine in antagonizing the contractile effects of St 587, clonidine and cirazoline on rat and guinea-pig aortas. No difference existed between the pA2 values of prazosin and yohimbine against the different agonists; the pA2 values of prazosin and yohimbine were significantly higher in rat aorta than those in guinea-pig aorta. The results can be explained by assuming the existence of two different agonist recognition sites on the alpha-1 adrenoceptor on rat aorta, whereas the alpha-1 adrenoceptor on guinea-pig aorta contains one agonist recognition site only. The architecture of the alpha-1 adrenoceptor on rat aorta must therefore be different from that in guinea-pig aorta.

Adrenergic alpha-Agonists↗
PubMed1980

[Mechanism of action of certain fibrinolytic bis-tetrahydroisoquinolines: their antagonists and histamine- and 5-hydroxytryptamine-releasing effects (author's transl)].

1, 1'-Heptamethylene-bis-6, 7-dimethoxy-1, 2, 3, 4-tetrahydroisoquinoline (HBDT) and 1, 1'-tetramethylene-bis-6, 7-dimethoxy-1, 2, 3, 4-tetrahydroisoquinoline (bisobrin) produced an edema when given subcutaneously into the hind paws of rats. The inhibitory effects of various antagonists on the paw edema and fibrinolysis induced by HBDT were examined in rats to determine whether chemical mediators other than histamine were involved. The relation of histamine to the fibrinolytic activity of these bis-tetrahydroisoquinoline derivatives has already been reported. Both edema and fibrinolysis were significantly inhibited by pretreatment with promethazine, cyproheptadine or phentolamine, but not by dibenamine, propranolol, atropine, indomethacin or pyridinolcarbamate. epsilon-Aminocaproic acid inhibited the fibrinolytic activity completely without any effect on the paw edema. HBDT released 5-hydroxytryptamine (5-HT) along with histamine from rat peritoneal mast cells. However, the amount of released 5-HT was considerably smaller than that of histamine. These results suggested that bis-tetrahydroisoquinolines released both histamine and 5-HT and that these mediators produced paw edema and induced fibrinolysis by enhancement of plasmin production.

Animals↗
PubMed1982

Recent advances in the purification of the alpha 1-adrenoceptor.

In order to purify the alpha-adrenergic receptor labeled with [3H]POB, antibodies against the irreversible alpha-adrenergic antagonist, phenoxybenzamine (POB), have been raised in rabbits immunized with POB conjugated to immunoglobulin. The antigen was prepared by first reacting POB with the sulfhydryl group of cysteine, after which the POB complex was coupled to thyroglobulin in the presence of water soluble carbodimide. POB-specific antibodies were first detected 10 days after the first booster injection. These antibodies display a high degree of specificity. Slight cross-reactivity occurred only with compounds structurally related to POB, such as dibenamine and nitrogen mustards, while catecholamines and alpha-adrenergic compounds not structurally related to POB did not cross-react, even when present in 100,000-fold excess. Moreover, the antibodies are still capable of recognizing POB once bound to alpha-adrenergic receptor. When membranes, prelabeled with [3H]POB, are solubilized with digitonin and incubated with anti-POB antiserum, the radioactivity can be specifically precipitated upon addition of goat anti-rabbit gamma-globulin serum. Thus these antibodies may be a useful tool in the purification of the alpha-adrenergic receptor of rat liver covalently linked to POB.

Animals↗
PubMed1982

Differences in histamine H1 and H2 receptor responses in several rabbit arteries.

Responses of helically cut segments from six different rabbit arteries to the selective histamine H1 receptor agonist 2-pyridylethylamine (PEA) and, in strips contracted by 10-4 M phenylephrine, to the selective histamine H2 agonist dimaprit have been determined. 10-3 M PEA contracted the renal artery, 96 +/- 2%; mesenteric artery, 92 +/- 2%; coeliac artery, 88 +/- 11% aorta 75 +/- 4%' ear artery 64 +/- 10% and pulmonary artery 48 +/- 5% of the maximal contraction to norepinephrine. 10-3 M dimaprit relaxed the phenylephrine contracted ear artery 48 +/- 8%; renal artery, 43 +/- 8%; coeliac artery 41 +/- 8%; mesenteric artery 36 +/- 5%; aorta 16 +/- 3%; and pulmonary artery 11 +/- 1% of the initial contractile tension. Strips in which histamine H1 receptors are blocked by 7 X 10-6 M mepyramine which are contracted by phenylephrine are partially relaxed by histamine. Cooling these strips markedly enhanced relaxations of the mesenteric and coeliac arteries but not those of the other four vessels. Exposure of the strips to dibenamine potentiated relaxations of all of the arteries except the ear artery and pulmonary artery. Thus there is heterogeneity among the arteries in their responses to histamine H1 and H2 receptor activation.

Animals↗
PubMed1982

A possible mechanism for elevation of glucose-6-phosphatase activity in kidney and liver of fluoride-treated rats.

Glucose-6-phosphatase (EC 3.1.3.9) activity in kidney and liver was found to be markedly elevated 3 hr after a single large dose of fluoride (NaF, 35 mg/kg, i.p.). The increases in renal and hepatic glucose-6-phosphatase activity were completely suppressed by adrenalectomy. Moreover, the increments were markedly suppressed by injection of dibenamine as an alpha-adrenergic blocker or by injection of propranolol as a beta-adrenergic blocker.

Adrenalectomy↗
PubMed1984

Direct and indirect actions of 5-hydroxytryptamine on the rat isolated vas deferens.

The contractile effect of 5-hydroxytryptamine on the rat isolated vas deferens was analyzed. In tissues from reserpine-pretreated animals 5-hydroxytryptamine (1 X 10(-6) M-3 X 10(-4) M) induced effects which were much lower than those induced in tissues from normal animals; the effects of low and medium concentrations of 5-hydroxytryptamine were antagonized by methysergide, those of medium and high concentrations were inhibited by phentolamine. In tissues from normal animals 5-hydroxytryptamine-induced contractions were compared with those induced by noradrenaline. 5-Hydroxytryptamine was less potent than noradrenaline and exhibited tachyphylaxis when the time interval between two successive exposures was too short. Phentolamine and dihydroergocristine reduced the effects of 5-hydroxytryptamine at concentrations lower than those necessary to antagonize noradrenaline-induced effects. Methysergide only reduced the effects of lower concentrations of 5-hydroxytryptamine. Cross-protection experiments showed that when noradrenaline was added before dibenamine, responses to both 5-hydroxytryptamine and noradrenaline were maintained to a very similar degree, while when 5-hydroxytryptamine was used as a protecting agent only a small degree of protection was found both towards noradrenaline and 5-hydroxytryptamine-induced effects. Cocaine potentiated the effects of low concentrations of 5-hydroxytryptamine while inhibiting those of high concentrations. The present study provides direct and indirect evidences that the contractile effect of 5-hydroxytryptamine on the rat vas deferens is prevailingly due to the release of noradrenaline; in the lower part of the concentration-response curve also direct effects are involved which are mediated by an interaction with both tryptaminergic "D" receptors and alpha 1-adrenoceptors.

Animals↗
PubMed1980

Toxicity and drug interactions of levamisole.

Clinical signs and lesions of levamisole toxicosis include: nausea, vomiting, increased salivation, frequent urination and defecation, colic, dizziness, headache, muscle tremors, ataxia, anxiety, hyperesthesia with irritability, clonic convulsions, depression, rapid respiration, dyspnea, prostration, collapse, hemorrhages in the subepicardium and thalamus, enteritis, hepatic degeneration and necrosis, and splenic congestion. Most of these signs and lesions are similar to those observed in nicotine poisoning. Levamisole causes vasopressor and panting effects which are blocked by ganglionic blocking agents hexamethonium and mecamylamine but are not blocked by atropine. The vasopressor effect of levamisole is blocked by alpha-adrenergic antagonists phentolamine and dibenamine; however, the respiratory effect of levamisole is not affected by these alpha-adrenergic antagonists. Repeated IV injections of levamisole cause a tachyphylactic response. With levamisole-induced tachyphylaxis, the effects of other ganglionic stimulants dimethylpiperazinium and nicotine are also abolished. Levamisole causes an electroencephalographic arousal which is antagonized by atropine sulfate and mecamylamine. There is also a structural similarity of levamisole to nicotine. These studies suggest that levamisole is a nicotine-like compound. Possible treatment of levamisole poisoning is discussed. Drug interactions of levamisole with organophosphates and anthelmintics, eg, pyrantel, methyridine, and diethylcarbamazine, are also discussed.

Animals↗
PubMedDate not supplied

[Nicotinamide coenzyme concentration in the myocardium of growing rats during alpha- and beta-adrenergic blockade].

The total content of oxidized (NAD+ plus NADP+) and reduced (NAD . H/ plus NADP . H2) forms of nicotinamide-adenine dinucleotides was detected in the myocardium of 7, 30-day- and 3--5 month-old (adult) noninbred white rats exposed to the alpha-adrenoblockers dibenamine and phentolamine (5 mg/kg) and to the beta-adrenoblockers anaprilin and alfeprol (1 mg/kg). It was shown that the content of nicotinamide coenzymes in the myocardium of growing rats exposed to different adrenoblockers changes depending on neurohumoral regulation and metabolism of the heart muscle within each age period.

Age Factors↗
PubMed1980

Protection against adrenochrome-induced myocardial damage by various pharmacological interventions.

Perfusion of the isolated rat heart with Krebs-Henseleit solution containing adrenochrome (25 or 50 mg/l), and oxidation product of catechalmines, resulted in contractile failure and myocardial necrosis. Various pharmacological agents known to protect the myocardium against catecholamine-induced necrosis were also found to be effective against adrenochrome-induced changes in the ultrastructure of the isolated perfused rat heart. The alpha-receptor-blocking drugs tolazoline and Dibenamine (dibenzylchlorethamine), and the adrenergic neurone-blocking agents guanethidine and bretylium did not alter the development of contractile failure and necrosis due to adrenochrome. The beta-receptor-blocking compounds propranolol and practolol effectively protected the heart from adrenochrome-induced necrotic damage, and partially prevented contractile failure. The hydrazine-type monoamine oxidase inhibitor iproniazid completely prevented ultrastructural damage and partially maintained contractile-force development in adrenochrome perfused hearts. The non-hydrazine-type monoamine oxidase inhibitor tranylcypromine partially protected the isolated rat heart against adrenochrome necrosis, but disruption of mitochondrial structure was still seen. Tranylcypromine did not significantly improve contractile force development during adrenochrome perfusion. The calcium antagonist D-600 reduced the severity of adrenochrome-induced ultrastructural damage. These results provide strong support for the view that catecholamine-induced cardiotoxicity is mediated through the formation of adrenochrome.

Adrenochrome↗
PubMed1980

The possible role of catecholamines in the protective effect of general anesthetics against kidney lesions in rats subjected to hemorrhagic hypotension.

Dibenamine, 15 mg/kg, injected i.p. in rats anesthetized with ketamine, 60 min before bleeding for 60 min against 40 mm Hg, significantly reduced the severity of kidney lesions. The maximum bleeding volume was reduced by 14%. Adrenalectomy also reduced the bleeding volume but all animals died within 24 hr. In unanesthetized rats bled against 40 mm Hg, plasma adrenaline and nor-adrenaline rose approximately tenfold as compared with unbled animals. Comparable marked increases in plasma adrenaline and somewhat smaller increases in plasma nor-adrenaline were observed after bleeding rats anesthetized with ketamine and ethylurethane, anesthetics which protect only slightly against the occurrence of kidney lesions. The rise in plasma adrenaline and nor-adrenaline was significantly lower after bleeding rats anesthetized with the highly protective anesthetics Na-pentobarbital, halothane and methoxyflurane. If, however, rats anesthetized with Na-pentobartical were bled for 40 min against 25 mm Hg, a situation in which the occurrence of kidney lesions is not prevented, the plasma concentration of both catecholamines was as high as in unanesthetized rats bled against 40 mm Hg. It is concluded that vasoconstriction due to the release of catecholamines is an important factor in the generation of kidney lesions during hypotension in rats and that the protective effect of a number of general anesthetics largely depends on their ability to suppress the release of catecholamines.

Adrenalectomy↗