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At least 523 records · Page 29Linked to original sources
PubMed1986

Brain regional [3H]flunitrazepam binding in rats chronically treated with bupropion or B.W.306U.

After 21 days of twice daily i.p. injections of bupropion (10 mg/kg), B.W.306U (10 mg/kg) or saline, 5 rat brain regions were removed for [3H]flunitrazepam binding assay. Scatchard analysis of the binding data revealed no change in the Bmax in any brain regions in drug-treated rats compared to controls. There was, however, a significant change in the Kd value in the limbic forebrain of B.W.306U-treated rats.

Animals↗
PubMed1988

Pharmacological studies in frog sympathetic ganglion: support for the cholinergic monosynaptic hypothesis for slow IPSP mediation.

The slow inhibitory postsynaptic potential (slow IPSP), the slow excitatory postsynaptic potential (slow EPSP), the late slow excitatory postsynaptic potential (late slow EPSP), and the fast excitatory postsynaptic potential/compound action potential (fast EPSP) were recorded from the 9th or 10th paravertebral sympathetic ganglia of bullfrogs (and some Rana pipiens frogs) by the sucrose-gap technique. The adrenergic antagonists phentolamine, dihydroergotamine and propranolol did not show any antagonistic effect on the slow IPSP when used at concentrations of up to 10, 100 and 10 microM, respectively. U-0521 (3',4'-dihydroxy-2-methylpropriophenone, 50 micrograms/ml), a specific inhibitor of catechol-O-methyltransferase, did not show any potentiating effect on the slow IPSP. The cholinesterase inhibitor neostigmine (0.5-1 microM) induced a large increase in the duration and amplitude of slow IPSP. When phentolamine and propranolol at concentrations greater than 10 microM were used the slow IPSP (and all other synaptic potentials) were non-specifically reduced in amplitude by these drugs. The results reported in this paper do not lend any support to the hypothesis that the slow IPSP in frog sympathetic ganglia is mediated by an adrenergic interneuron. The results are consistent with the proposal that the slow IPSP in this ganglion is mediated by a direct action of acetylcholine released from cholinergic preganglionic fibers.

Action Potentials↗
PubMed1975

Further study of the adrenoceptors of the saphenous vein of the dog: influence of factors which interfere with the concentrations of agonists at the receptor level.

In the present study the affinities of some sympathomimetic amines for alpha- and beta-adrenoceptors of the dog saphenous vein tissue were determined after all known factors interfering with the concentration of these agonists at the receptor level had been assessed and excluded. It was observed that in control experiments the relative potencies of sympathomimetic agonists for inducing contractions were: adrenaline (1.6) greater than noradrenaline (1.0) greater than phenylephrine (0.38) greater than isoprenaline (0.009). The elimination of neuronal uptake by cocaine, 4 X 10(-6) M, enhanced predominantly the effects of noradrenaline (by a factor of 7.5), whereas block of catechol-O-methyl transferase (COMT) by U-0521, 10(-4) M, only enhanced those of adrenaline (by a factor of 2.6) and block of beta-adrenoceptors by propranolol, 5 X 10(-7) M, enhanced those of isoprenaline (by a factor of 3) and adrenaline (by a factor of 1.8). Block of COMT enhanced the effects of adrenaline approximately as much as did the blockade of neuronal uptake; this seems to indicate that the affinity of adrenaline for extraneuronal and neuronal uptake processes is approximately the same. Regarding the relaxation-inducing capacity of sympathomimetic agents it was observed that isoprenaline, adrenaline and noradrenaline are full agonists, whereas phenylephrine was not able to produce relaxation amounting to more than 5% of the maximum. Denervation did not modify the relaxant effects of isoprenaline. After elimination of all known factors interfering with the concentration of the sympathomimetic agonists in the biophase, the ratios between the ED50's of each amine for alpha- and beta-adrenoceptors were: adrenaline = 34, noradrenaline = 109 and isoprenaline = 0.0041.

Animals↗
PubMed1978

Vascular and myocardial effects of mecinarone.

The effects of mecinarone on the contractions induced by noradrenaline, potassium and calcium were studied with the isolated aorta and central artery of the rabbit ear. In our experimental conditions mecinarone was found to act as a competitive antagonist of calcium. It preferentially inhibited the noradrenaline-evoked contraction induced in the rabbit ear artery and had a smaller effect on the extracellular calcium-induced contraction of depolarized arterial smooth muscle. In the isolated guinea pig heart, mecinarone produced a reversible decrease in the rate of rise of the ascendant phase of the action potential without significantly changing the resting potential. In hearts inactivated by depolarisation, mecinarone inhibited the contractions restored by isoproterenol without suppressing the calcium action potential. These results suggest that the mode of action of mecinarone is different from that of verapamil or nifedipine but is comparable to that of chlorpromazine, although mecinarone has no sedative effect.

Action Potentials↗
PubMed1981

An alpha-adrenoceptor inhibitory action of kynuramine.

Kynuramine, an endogenously occurring amine, inhibited the vasoconstrictor responses to norepinephrine in the isolated perfused mesenteric arteries of rats and blocked the relaxation of rabbit intestinal smooth muscle by phenylephrine. Similarly, kynuramine reversed clonidine-induced inhibition of the cholinergic twitch response in the guinea pig ileum. These effects, seen with concentration ranging from 4 to 60 microgram/ml, are consistent with an alpha-adrenoceptor inhibitory action of kynuramine at both presynaptic and postsynaptic sites. Kynuramine itself, lacked intrinsic activity on alpha-adrenoceptors and showed a complete lack of affinity for beta-adrenoceptors in the rabbit intestine and guinea pig tracheal chain preparation. None of the effects of kynuramine could be attributed to the formation of 4-hydroxyquinoline, the deaminated metabolite of kynuramine. Additionally, no evidence was obtained for an action on muscarinic receptors or non-specific effects on vascular smooth muscle. However, a slight, transient stimulant action was evident on intestinal smooth muscle. It is concluded that kynuramine inhibits both presynaptic and postsynaptic alpha-adrenoceptors in vitro and it is conceivable that the compound might function as an endogenous inhibitor of alpha-adrenoceptors in vivo.

Adrenergic alpha-Antagonists↗
PubMed1983

Blood pressure and heart rate effects of kynuramine in pithed rats.

Kynuramine increased heart rate and blood pressure in pithed rats. Heart rate responses were blocked by beta-adrenoceptor antagonists and reserpine pretreatment. Both of these treatments reduced the pressor responses to kynuramine. Remaining pressor activity was inhibited by phentolamine. The pressor responses to kynuramine were reversed to depressor responses during infusion of norepinephrine but not vasopressin. It is concluded that kynuramine releases cardiac catecholamines and acts as a partial agonist on vascular alpha-adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed1984

Kynuramine: high affinity for [3H]tryptamine binding sites.

Kynuramine, an endogenously occurring metabolite of L-tryptophan, was found to displace [3H]tryptamine from its high affinity binding sites in rat brain cortex with an inhibition constant (Ki) of 28 nM. Kynuramine exhibited structural specificity and considerable selectivity, compared with its affinity for serotonergic, adrenergic and benzodiazepine recognition sites. This novel finding opens-up the possibility that kynuramine may exert physiological actions via the putative tryptamine receptor.

Animals↗
PubMed1984

Effect of propafenone on the membrane currents of rabbit sino-atrial node cells.

The effects of propafenone (1-50 micrograms/ml) on the membrane potential and currents of the rabbit sino-atrial node were studied using the voltage clamp technique. Propafenone decreased the heart rate, amplitude of the action potential and maximum rate of depolarization. It also depolarized the maximum diastolic potential and the resting potential and prolonged the action potential duration dose dependently. On the current systems of the sino-atrial node, propafenone reduced the outward current (ik), the inward current activated by hyperpolarization (ih) and the slow inward current (is) dose dependently. The decrease in is and ik by propafenone was due to the reductions in their conductance, not to the changes in the voltage dependence of the inactivation of is or activation of ik. The decrease in ik might be the ionic mechanism of the negative chronotropic effect of propafenone.

Action Potentials↗
PubMed1984

Affinity changes of rat striatal dopamine receptors in vivo after acute bupropion treatment.

The effect of bupropion (Wellbutrin) was studied on in vivo [3H]spiperone binding in rat striatum and cerebellum. The compound increased binding dose dependently in striatum whereas no effect was observed in cerebellum. Saturation analyses of in vivo binding in the striatum revealed an increased affinity of the receptors rather than changes in the number of binding sites. These results are the first demonstration of an increased sensitivity of central dopamine receptors after acute bupropion treatment.

Animals↗
PubMed1985

Electrophysiological effects of propafenone on isolated guinea-pig ventricular muscle and sheep Purkinje fibres.

The electrophysiological effects of propafenone on transmembrane potentials were studied in sheep Purkinje fibres and guinea-pig ventricular muscle. In both preparations propafenone decreased the amplitude and Vmax of the action potential and shifted the resting membrane potential to less negative values. In Purkinje fibres, propafenone also slowed the conduction velocity and shortened the action potential duration whereas in ventricular muscle it had no effect on action potential duration. Propafenone also suppressed: the normal automatic mechanism in Purkinje fibres as well as the automaticity induced by BaCl2 and isoprenaline in ventricular muscle fibres with high resting membrane potential (between -75 mV and -85 mV), the abnormal automatic mechanisms, including the slow action potentials induced by BaCl2 and isoprenaline in ventricular muscle and Purkinje fibres depolarized above -55 mV, respectively, and the delayed after-depolarizations induced by ouabain in Purkinje fibres and ventricular muscle. The possible mechanisms responsible for the cardiac effects of propafenone and the therapeutic implications of these electrophysiological effects are discussed.

Action Potentials↗