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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The beta-adrenomimetic and beta-adrenolytic activities of S(-) and R(+) isomers of carteolol, a beta-adrenergic partial agonist (a beta-adrenoceptor blocker with intrinsic sympathomimetic action) were tested in the guinea-pig taenia caecum. 2. The beta-adrenoceptor blocking activities (pA2 values) of S(-) and R(+) isomers of carteolol were significantly larger than the corresponding beta-adrenomimetic activities (pD2 values), supporting our views that beta-adrenoceptors contain two different binding sites; high and low affinity sites. 3. In beta-adrenoceptor blocking action S(-) carteolol was about 10 times as potent as R(+) carteolol while beta-adrenomimetic action of S(-) carteolol was about 2 times as potent as that of R(+) carteolol. Further, intrinsic activity for S(-) carteolol was slightly but significantly larger than that for R(+) carteolol. 4. These results suggest that the binding site for competitive antagonism between S(-) isoprenaline and S(-), R(+) and RS(+/-) carteolol is more stereoselective than the binding site to induce beta-adrenomimetic action.
Gen Pharmacol 1990
PMID:Stereoselectivity in beta-adrenomimetic and beta-adrenolytic actions of carteolol, a beta-adrenoceptor blocker with intrinsic sympathomimetic action in guinea-pig taenia caecum. 197 Dec 47

1. Isoprenaline, a beta-adrenergic full agonist, and carteolol, befunolol and BFE-55, beta-adrenergic blockers with an intrinsic sympathomimetic action, induced dose-related increases in heart rate when administered intravenously (i.v.). 2. The beta-partial agonists administered i.v. shifted a dose-heart rate increased response curve of isoprenaline, suggesting a competitive antagonism. 3. In carteolol, doses to block beta-adrenoceptors were found to be 400-1000 times lower than that to induce agonistic action. In BFE-55, doses to block beta-adrenoceptors were equal to that to induce sympathomimetic action. The difference between doses of the befunolol to produce both actions was intermediate. 4. These results suggest that there may be a difference between doses blocking beta-adrenoceptors and inducing sympathomimetic action in some beta-adrenergic partial agonists and, therefore, that there may exist beta-partial agonists which do not induce sympathomimetic action in doses blocking beta-adrenoceptors.
Gen Pharmacol 1989
PMID:Dose difference in beta-adrenergic blockers with intrinsic sympathomimetic action to block beta-adrenoceptors and induce sympathomimetic action. 256 66

A beta-adrenoceptor blocking agent, befunolol, which is clinically used in the treatment of glaucoma in Japan, was found to have intrinsic sympathomimetic activities in isolated right atria, trachea and taenia caecum of guinea pig (intrinsic activities are 0.22-0.28). The pD2-values of befunolol estimated in the isolated organs were significantly different from its pA2-values against isoprenaline. A possible explanation of our findings would to be as follows: befunolol interacts with the beta-adrenoceptor where there may be two different sites: one site for agonistic action and the other for competitive antagonistic action. Both sites are supposed to be mutually exclusive through unknown mechanisms. The intrinsic activity of befunolol may be equal to its selectivity for both the sites.
Gen Pharmacol 1985
PMID:A beta-adrenoceptor blocking agent, befunolol as a partial agonist in isolated organs. 286 92

To investigate the involvement of adrenergic mechanisms in the development of obesity, hyperglycaemia and hyperinsulinaemia in Aston ob/ob mice, the sympathomimetic agent ephedrine (12 mg/kg/day) and the predominantly beta 1-adrenergic antagonist atenolol (12 mg/kg/day) were administered alone and in combination to weanling ob/ob mice for 40 days. Excessive weight gain in ob/ob mice was reduced (15-20%) by ephedrine, exacerbated (8-10%) by atenolol, but not significantly altered by a combination of these agents. The effects of ephedrine and atenolol were lost rapidly (within 5 days) when these agents were withdrawn. Ephedrine slightly reduced the hyperphagia in ob/ob mice, and food intake was transiently increased above that of untreated ob/ob mice when this agent was withdrawn. The development of basal hyperglycaemia and hyperinsulinaemia was not significantly altered by any of the treatments studied. None of the treatments significantly altered body weight, food intake, plasma glucose or plasma insulin concentrations in lean (+/+) mice. The results indicate that a defective adrenergic mechanism involving beta 1-adrenergic receptors contributes to the development of obesity in ob/ob mice.
Gen Pharmacol 1986
PMID:Effects of ephedrine and atenolol on the development of obesity and diabetes in ob/ob mice. 351 92

The action potential duration (APD) of isolated guinea pig papillary muscle is directly related to the medium glucose concentration regardless of the gas mixture with which it is in equilibrium. The APD can be maintained at control value for many hours by a glucose concentration of 50 mM in the complete absence of oxygen. Following reduction of the APD by incubation of the muscle in medium containing 5 mM glucose, adjustment of the glucose concentration to 50 mM will cause restoration of normal APD. Phlorizin has been shown to competitively interfere with the effect of glucose on the APD and insulin to prevent or reverse the effect of phlorizin. Nonmetabolizable sugars cannot produce glucose-like effects on the APD. Adrenaline, noradrenaline, and isopropylnoradrenaline increased the reduced APD of papillary muscles incubated in the absence of oxygen in a medium containing 5 mM glucose coincident with an increase in contractile force. The effect of isopropylnoradrenaline was blocked by acetylcholine and propranolol. In the presence of iodoacetate and 2-deoxyglucose, isopropylnoradrenaline increased contractile force but not the reduced APD. Aminophylline was found to produce changes in the reduced APD similar to those caused by the sympathomimetic amines. The findings clearly support the hypothesis that anaerobic metabolism utilizing either glycogen or exogenous glucose is capable of maintaining normal transmembrane electrical activity in guinea pig papillary muscle.
J Gen Physiol 1969 Jun
PMID:Influence of glucose on the transmembrane action potential of papillary muscle. Effects of concentration, phlorizin and insulin, nonmetabolizable sugars, and stimulators of glycolysis. 578 11

In dog mesenteric arteries, nialamide (10(-5) M), a monoamine oxidase inhibitor, potentiated contractile response to tyramine but not to noradrenaline or transmural electrical stimulation (TES). Bretylium, desipramine or prior reserpinization inhibited the potentiating action of nialamide on the tyramine-induced contraction. Contractions induced by octopamine were not reduced by prior reserpinization. In the coronary artery, relaxing responses to tyramine were potentiated but those to noradrenaline and TES were not potentiated by nialamide. In the cerebral artery, nialamide failed to potentiate tyramine-induced contraction. The functional role of intraneuronal monoamine oxidase in sympathomimetic effects is discussed.
Gen Pharmacol 1984
PMID:Effects of nialamide on responses of dog isolated arteries to tyramine and transmural electrical stimulation. 642 49

The elevated serum gonadotropin (GtH) levels in goldfish receiving two injections of des Gly10, [D-Ala6] LH-RH ethylamide (LH-RH-A), given 12-hr apart, were reduced by apomorphine, a dopamine agonist, injected at either the first or the second LH-RH-A injection. Serum GtH concentrations in goldfish given two injections of LH-RH-A at a 3-hr interval were also depressed by bromocriptine, a specific D-2 dopamine receptor agonist, administered simultaneously with both LH-RH-A injections. Injections of dopamine antagonists, pimozide or metoclopramide (a specific D-2 antagonist) caused increased serum GtH concentrations in normal goldfish, but no changes were found following injections of the alpha-adrenergic antagonist phentolamine, the beta-adrenergic antagonist propranolol, or the sympathomimetic agent octopamine. Injection of pimozide or metoclopramide at the time of the second of two LH-RH-A injections given at an interval of 12 hr potentiated the LH-RH-A-induced increase in serum GtH concentrations; injections of phentolamine, propranolol, or octopamine did not alter the response to LH-RH-A. Injections of pimozide or metoclopramide also increased the frequency of ovulation in LH-RH-A-injected gravid female goldfish. These results suggest that stimulation of dopamine receptors can block the potentiating effect of multiple injections of GtH-releasing hormone, as well as ongoing LH-RH-A-stimulated release. The results also indicate that the dopamine inhibition of GtH secretion is specific and may be mediated by receptors resembling the D-2 type receptors in mammals.
Gen Comp Endocrinol 1984 Sep
PMID:Effects of catecholaminergic agonists and antagonists on serum gonadotropin concentrations and ovulation in goldfish: evidence for specificity of dopamine inhibition of gonadotropin secretion. 643 24

Pindolol is a non-selective beta-adrenoceptor blocking agent with relatively marked intrinsic sympathomimetic activity. Stimulant effects in isolated, perfused mesenteric vessels (beta 2) equal those of isoprenaline. Effects on guinea-pig atria (beta 1) are negligible and those on guinea-pig trachea (beta 1 and beta 2) and cat atria (beta 1 and beta 2) are equivalent to 40-50% of the maximum effects of isoprenaline. It is concluded that the intrinsic sympathomimetic activity of pindolol is exerted principally on the beta 2-adrenoceptor. The beta-adrenoceptor blocking effect of pindolol is largely confined to the (-)enantiomer, whereas its stimulant effects are shared equally by the (+) and (-)enantiomers. Removal of the side chain hydroxyl group of pindolol does not diminish stimulant activity, but abolishes blocking activity. Pindolol-induced stimulation and blockade of beta-adrenoceptors may be brought about by different configurations of the molecule. Vasodilator effects observed in vitro and in vivo suggest that beta-adrenoceptor stimulation may make an important contribution to the antihypertensive effect of pindolol in man.
Gen Pharmacol 1983
PMID:Effects of pindolol on vascular smooth muscle. 682 21

1. The distribution of sympathetic nerves in hand arteries and veins from 18 normal subjects was studied by microscopy according to the Falck-Hillarp histofluorescence method for the cellular visualization of cathecholamines and by quantitative analysis of noradrenaline with a radioenzymatic method. Segments of hand arteries and veins were tested in vitro for the vasomotor effect of sympathomimetic agonists. 2. Fluorescence microscopy revealed a plexus of noradrenaline-containing nerve fibres surrounding both arteries and veins. The concentration of noradrenaline in the walls were 4.5-4.7 ng/mg protein. The relative agonist potency was characteristic for alpha-receptors. Phentolamine produced parallel shift of the dose-response curves both for arteries and veins. 3. Finger plethysmography with local cold provocation down to 10 degrees C was performed in the patients with traumatic vasospastic disease before and after inhibition of the sympathetic nervous system by body warming and orally administered alcohol. Four patients had undisturbed circulation, as revealed by the ratio between the systolic blood pressure in the arm and in the finger in conjunction with cold provocation tests. 13 patients had vasospasm of varying degrees, and 3 patients suffered from organic stenosis. 4. Hand angiography was performed before and after local cold provocation. The patients with organic stenosis did not show vasodilatation after 4-6 mg phentolamine injection. Patients with true vasospasm responded, in addition, with efficient vasodilatation 15 min after reserpine injection, which also abolished the cold-induced vasospasm.
Gen Pharmacol 1983
PMID:Analysis of vasospasm in hand arteries by in vitro pharmacology, hand angiography and finger plethysmography. 682 38

1. We tested the novel thiazole derivative, amthamine, for its ability to stimulate histamine H2-receptors in the human myocardium. 2. Experiments were carried out on isolated, electrically-driven pectinate muscle segments, excised from atrial appendages of patients undergoing corrective heart surgery. 3. Amthamine (0.3-100 microM) induced a positive inotropic activity, resembling histamine in terms of potency and efficacy. In comparison, impromidine was 10-30 times more active than histamine and amthamine, but its maximum effect was significantly lower, while dimaprit was as effective as histamine, but 10 times less potent. 4. The selective histamine H2-blocker, famotidine antagonized in a competitive fashion the amthamine-induced positive inotropic effect. pA2 value of famotidine against amthamine (7.21 +/- 0.45) was close to that measured against histamine (6.88 +/- 0.31) in the same conditions. 5. The effect of amthamine was not modified by beta-adrenoceptor blockade, excluding direct or indirect sympathomimetic activities of the compound. 6. These data provide evidence that amthamine is a selective and full acting histamine H2-receptor agonist in the human heart in vitro.
Gen Pharmacol 1994 Dec
PMID:Positive inotropic activity of the novel histamine H2-receptor agonist, amthamine, on the human heart in vitro. 772 Oct 41


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