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At least 721 records · Page 40Linked to original sources
PubMed1975

An indirect sympathomimetic effect of burimamide on kitten isolated atria.

1. Burimamide (34-1080 muM) caused a concentration-dependent increase in the force and frequency of contraction of kitten isolated atria. 2. Metiamide (467 muM) had no stimulant action on kitten atria and did not modify the effects of burimamide. 3. The atrial stimulation produced by burimamide was reduced by (-)propranolol (34-68 nM) and by cocaine (3 muM). 4. The atrial stimulant effect of burimamide was prevented by pretreatment of kittens with reserpine (1 mg/kg, 24 h before the experiment). 5. It is concluded that burimamide causes atrial stimulation by releasing catecholamines.

Animals↗
PubMed1976

Effects of sympathomimetic amines on 45Ca efflux from liver slices.

The efflux of 45Ca from slices of guinea-pig and rabbit liver is greatly increased by alpha-adrenoceptor agonists. Isoprenaline is much less effective. The effects of these agents on the efflux of 45Ca mirror their actions on 42K loss and suggest that the two may be related. Glucose release from both rabbit and guinea-pig liver slices is increased to a similar extent by either alpha- or beta-receptor agonists. The possible relationship between Ca and K movements and the production of glucose is discussed.

Animals↗
PubMed1980

alpha-Sympathomimetic amines and calcium-mediated action potentials in guinea-pig ventricular muscle.

1 The ability of amines, having alpha- or alpha- and beta-adrenoceptor stimulating activity, to restore excitability and contractility in heart preparations partially depolarized by potassium, was investigated in guinea-pig ventricular muscle in order to elucidate the mechanism of the positive inotropic effect mediated via alpha-adrenoceptors. 2 In preparations in which fast sodium channels were inactivated by K+-rich medium (22 mM) slow electrical responses as well as contractions were consistently induced by high concentrations of phenylephrine (10(-4) to 3 X 10(-4) M) and synephrine (3 X 10(-4) M). 3 The restorative effective effects of both phenylephrine and synephrine were unaffected by phentolamine (10(-5) M) but were readily abolished by practolol (10(-5) M) or sotalol (10(-5) M). 4 Methoxamine induced a dose-dependent positive inotropic effect in ventricular strips paced at 0.5 Hz in normal Tyrode solution; the maximum increase in contractile tension was obtained with methoxamine 10(-4) M. However, at the same concentration, the amine did not induce slow electrical responses in potassium-depolarized preparations. 5 It is concluded that the induction of slow responses by phenylephrine and synephrine is due to beta-adrenoceptor stimulation, and that the increase in cardiac contractility caused by alpha-adrenoceptor stimulation does not involve an increase in slow inward calcium current.

Action Potentials↗
PubMed1983

Effects of LM 5008, a selective inhibitor of 5-hydroxytryptamine uptake, on blood pressure and responses to sympathomimetic amines.

LM 5008 (4-[2-(3-indolyl)ethyl]piperidine) (10, 20 and 50 mg kg-1) had no significant effect on pressor responses to noradrenaline or tyramine in rats anaesthetized with urethane. Desmethylimipramine (1 mg kg-1) blocked the response to tyramine but chlorimipramine (5 mg kg-1) had no significant effect on responses to noradrenaline or tyramine. In the rabbit, anaesthetized with chloralose, LM 5008 (5 mg kg-1) had no effect on pressor responses to noradrenaline, tyramine or angiotensin II, while desmethylimipramine (0.25 mg kg-1) inhibited responses to tyramine and potentiated those to noradrenaline. LM 5008 (10 mg kg-1) had no effect on resting blood pressure of conscious normotensive or DOCA-saline hypertensive rats. Tranylcypromine (5 mg kg-1) produced a fall in blood pressure in conscious normotensive and in DOCA hypertensive rats. Treatment with a combination of LM 5008 (10 mg kg-1) and tranylcypromine (5 mg kg-1) resulted in the appearance of a behavioural hyperactivity syndrome, but blood pressure was not different from that of animals treated with tranylcypromine alone. These results further demonstrate the selectivity of LM 5008 for 5-hydroxytryptamine as opposed to catecholamine uptake.

Angiotensin II↗
PubMed1988

4-Hydroxy-2-methyl-4-phenyl-1,2,3,4-tetrahydroisoquinoline (PI-OH): a new potentiator of sympathomimetic amines on the rat anococcygeus muscle.

1. The potentiating effects of racemic 4-hydroxy-2-methyl-4-phenyl-1,2,3,4-tetrahydroisoquinoline (PI-OH), cocaine, desipramine and nomifensine on the concentration-response curves of the rat anococcygeus muscle to noradrenaline (NA) and field stimulation were examined. 2. PI-OH and cocaine concentration-dependently potentiated the responses of anococcygeus muscle to NA and field stimulation, but the activity of PI-OH was stronger than that of cocaine on both responses. 3. At high concentrations the potentiating activities of desipramine and nomifensine were less, a fact that was explained by their postsynaptic inhibitory properties; the actions of nomifensine and desipramine as antagonists against NA were competitive and non-competitive, respectively. 4. It is concluded that PI-OH may be an ideal potentiator of the response to NA in adrenergically-innervated tissues because it has no side effects such as postsynaptic inhibition.

Animals↗
PubMed2006

Sympathomimetic infusion and cardiac repolarization: the normative effects of epinephrine and isoproterenol in healthy subjects.

INTRODUCTION: Catecholamines are known to affect cardiac repolarization, and provocation with either isoproterenol or epinephrine has been proposed as a tool for uncovering latent repolarization abnormalities. This study systematically compares the effects of isoproterenol and epinephrine infusions on QT interval (QT), T waves and U waves in normal subjects. METHODS AND RESULTS: Twenty-four normal subjects (29 +/- 8 years) were evaluated during graded infusions of up to 0.30 microg/kg/minute epinephrine and 5.0 microg/minute isoproterenol. Heart rates at peak doses were 81 +/- 13 bpm at 0.28 +/- 0.04 microg/kg/minute epinephrine and 104 +/- 5 bpm at 2.4 microg/minute isoproterenol. The longest absolute QT increase was 4 +/- 5 msec above baseline during isoproterenol (P < 0.001) and 12 +/- 23 msec during epinephrine (P = 0.07), while the longest corrected QT interval (QTc) increase was 67 +/- 28 msec (P < 0.0001) and 79 +/- 40 msec (P < 0.0001) above baseline during isoproterenol and epinephrine, respectively (P = 0.12 for difference). There was a 2-fold increase in U-wave amplitude during each intervention (P < 0.001). The specificity of paradoxical QT prolongation (>or=30 msec at 0.05 microg/kg/minute or >or=35 msec at 0.10 microg/kg/minute epinephrine) and an increase in QTc >or=600 msec at any dose epinephrine were 100%. However, the specificity of other proposed criteria that utilized QTc measurement (>or=30 msec at 0.10 microg/kg/minute or >or=65 msec at any dose) was poor whether all leads or only lead II were assessed. CONCLUSION: Both epinephrine and isoproterenol are associated with QTc prolongation and amplification of the U wave in normal subjects. The specificity of proposed criteria for epinephrine provocation in diagnosis of the long-QT syndrome is variable; however, paradoxical QT prolongation at low-dose epinephrine or a QTc >or=600 msec is highly specific.

Adult↗