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At least 1,387 records · Page 77Linked to original sources
PubMed1983

Release of norepinephrine from organ-cultured superior cervical ganglia: effects of the norepinephrine uptake inhibitor xylamine.

After preloading with [3H]norepinephrine (NE), organ-cultured superior cervical ganglia released increased amounts of [3H]NE when incubated with depolarizing K+ concentrations, tyramine or amphetamine. K+-induced release was Ca++-dependent, whereas tyramine- and amphetamine-induced release were not. Analysis of the released radioactivity by high-pressure liquid chromatography showed that these releasing stimuli caused primarily an increase in NE release, with little increase in the release of NE metabolites. Incubation with 10 microM xylamine, an irreversible inhibitor of NE uptake, caused a small increase in [3H]NE efflux, but no reduction in the endogenous NE and dopamine levels in superior cervical ganglia. After xylamine treatment, tyramine-induced release was greatly inhibited, whereas release by amphetamine and K+ was not. The neuronal uptake inhibitor desipramine (1 microM), affected K+-, tyramine- and amphetamine-induced release in a manner similar to xylamine. It is concluded that xylamine is a very weak releasing agent in this tissue and that its effects on other release processes are consistent with its action as a NE uptake inhibitor. Amphetamine-induced release appears not to require the NE uptake system for either the uptake of amphetamine, as shown by the accumulation of [3H]amphetamine, or the efflux of NE.

Animals↗
PubMed2000

Evidence of the dual mechanisms of action of venlafaxine.

BACKGROUND: Indirect evidence suggests that the antidepressant venlafaxine hydrochloride selectively inhibits serotonin (5-HT) uptake at low doses, whereas at high doses, it inhibits both 5-HT and norepinephrine (NE) uptake. We hypothesized that, in vivo, both high and low doses would inhibit the 5-HT uptake of platelets but that the higher dose would differentially blunt the pressor response to tyramine, a marker for NE uptake. METHODS: Healthy male volunteers aged 18 to 45 years received either 75 mg or 375 mg of venlafaxine hydrochloride per day, the 5-HT uptake inhibitor sertraline hydrochloride (50 mg/d), or the NE uptake inhibitor maprotiline hydrochloride (150 mg/d) (n = 8 for each of 4 treatment groups). Changes in platelet 5-HT uptake and the pressor response to intravenous tyramine were assessed following the initial dose and after 1 and 2 weeks of drug administration. RESULTS: Platelet 5-HT uptake was inhibited by venlafaxine across the dose range and by sertraline but not maprotiline. Inhibition was competitive, related to increases in affinity and not related to capacity. Steady-state drug levels were associated with a 5-HT uptake inhibition of 87% or more in subjects taking venlafaxine or sertraline. The pressor response to tyramine differentially distinguished maprotiline from sertraline and the low dose of venlafaxine but not from the high dose of venlafaxine. CONCLUSION: This study provides the first in vivo evidence in healthy humans that both 5-HT uptake and NE uptake inhibition are mechanisms of action sequentially engaged by venlafaxine over its clinically relevant dose range.

Adolescent↗
PubMed2006

Changes in fluid secretion rate alter net transepithelial transport of MRP2 and P-glycoprotein substrates in Malpighian tubules of Drosophila melanogaster.

The effects of stimulants of fluid secretion on net transepithelial transport of the MRP2 substrate Texas Red and the p-glycoprotein substrate daunorubicin were examined in Malpighian tubules of Drosophila melanogaster. Fluid secretion rates were determined using the Ramsay assay and secreted fluid concentrations of Texas Red and daunorubicin were determined using a microfluorometric technique. Nanoliter droplets of secreted fluid were collected in optically flat glass capillaries and dye concentration was determined from fluorescence intensity measured by confocal laser scanning microscopy. Net transepithelial flux of each compound was then calculated as the product of its concentration in the secreted fluid and the fluid secretion rate. Net transepithelial flux of Texas Red increased when fluid secretion was stimulated by tyramine, cyclic AMP or hypoosmotic saline. Net flux decreased when fluid secretion rate of cAMP-stimulated tubules was reduced by elevating saline osmolality with sucrose. Net transepithelial flux of daunorubicin increased when fluid secretion was stimulated by cAMP. Significant increases in dye flux were seen only when the dyes were present at concentrations close to or greater than the concentration required for half maximal transport. Regression analyses showed that 57- 88% of the change in dye flux was attributable to the change in fluid secretion rate when tubules were stimulated with cAMP, cGMP, or tyramine. The results do not suggest that the effects of tyramine and cAMP are mediated through changes in transepithelial potential, nor do they indicate the direct effects of the stimulants on MRP2-like or p-glycoprotein-like transporters (e.g., via protein kinases). Instead, the results suggest that increases in fluid secretion rate minimize diffusive backflux of these dyes and, thus, facilitate higher rates of net transepithelial transport indirectly.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed1979

Some new fluorescent derivatives for the mass spectrometric quantitation of biogenic amines.

The 5-dimethyl-, diethyl-, dipropyl-, dibutyl-, and dipentyl-aminoaphghalene-1-sulfonyl (dansyl, ethanyl, propansyl, bansyl and pentansyl respectively) derivatives of tyramine and other biogenic amines were prepared and their mass spectra recorded. The relative intensity of the largest unique ion increased with increasing length of the alkyl group. Several O-alkyl-N-propansyl- and N,O-dialkyl-N-propansyl-, bansyl- and pentansyl-tyramines were also synthesized and their mass spectra recorded. Dimethylbansyl- and dimethylpentansyl-tyramines exhibited the largest unique ions in their mass spectra and the greatest sensitivity in quantitation by the integrated ion current method. Procedures for preparing these derivatives in amounts ranging from nanograms to milligrams are presented and their thin-layer chromatographic behavior in three solvent systems is described.

Biogenic Amines↗
PubMed1991

PC12 cells as a window for the differentiation of neural crest into adrenergic nerve ending and adrenal medulla.

Studies on PC12 and isolated adrenal chromaffin cells have revealed that PC12 cells have a closer identity to the adrenergic nerve ending than do the chromaffin cells. This is revealed by the presence of monoamine oxidase (MAO) A and tyramine-released pool of catecholamines in PC12, resembling that in adrenergic neurones, and their absence in adrenal chromaffin cells. Indeed, chromaffin cells possess primarily MAO-B activity. Like the observations on adrenergic neurones, non-selective and selective MAO-A inhibitors potentiate the catecholamine-releasing property of tyramine in PC12 cells. This property has clearly been demonstrated to be associated with selective inhibition of MAO-A and not MAO-B. The fact that MAO-A and MAO-B are different proteins and under separate gene product control suggests that their regulation may be highly differentiated. Indeed, it has been shown that while steroids such as progesterone and hydrocortisone induce and estrogen diminishes MAO-A activity in PC12 cells, no such regulatory mechanism has been identified for MAO-B activity in chromaffin cells. In the final analysis the inter-relationship between MAO-A activity and the presence of tyramine-releasable pool of catecholamines in adrenergic neurons and PC12 cells may have a genetic basis and could be important in illuminating the differentiation of neural crest into adrenergic neurones and adrenal medulla on the one hand and chromaffin cells to PC12 cells on the other.

Adrenal Medulla↗
PubMed1995

Okadaic acid modulates exocytotic and transporter-dependent release of dopamine in bovine retina in vitro.

Bovine retinas were isolated for the study of the modulation of exocytotic and transporter-dependent release of dopamine (DA) in vitro. Endogenous DA was measured in the medium using HPLC with electrochemical detection under successive incubations with transfers in fresh medium every 30 min. As expected, potassium caused a calcium-dependent exocytotic liberation of DA. Amphetamine or tyramine induced a calcium-independent release by reversing DA transport across the plasma membrane. Okadaic acid, a specific inhibitor of phosphatases 1 and 2A, induced a slight but significant DA release in the absence of calcium. Furthermore, the toxin increased potassium-, amphetamine- or tyramine-induced DA release independently of extracellular calcium. In addition, okadaic acid completely annulled the ability of a calcium-free extracellular environment to inhibit the potassium-induced DA release. Finally, the toxin prevented the time-dependent decline in the efficacies of amphetamine or tyramine to release DA. In agreement with proposed schemes described for rat striatum, the results of the present study confirmed the existence of distinct release modes of DA in bovine retina. The results obtained with okadaic acid suggest that phosphatase 1 and/or phosphatase 2A constitute part of a direct or indirect mechanism to inhibit both exocytotic and transporter-dependent DA release.

Animals↗
PubMed1977

Substrate-typic changes of platelet monoamine oxidase activity in sub-types of schizophrenia.

Monoamine oxidase (MAO) activity has been measured in the platelets of controls (n = 42) and schizophrenic patients (n = 49) of three subtypes, using beta-phenylethylamine, p-tyramine, and tryptamine as substrates. Characteristic differences of MAO activity were observed between platelets of patients and controls; the differences were substrate-typic: decreased enzyme activity was found with all three substrates in platelets of the parnaoid subtype. With tryptamine, MAO activity was decreased in the platelets of all three sub-types of schizophrenia. With p-tyramine, MAO was low in patients with affective psychoses and paranoid schizophrenia. The value of MAO activity measurements as a means for distinguishing sub-types of schizophrenic disorders is improved by using two substrates; tryptamine and p-tyramine. Possible mechanisms of the substrate-typic changes of platelet MAO activity in schizophrenia are discussed.

Adult↗
PubMed1977

Noradrenaline, depressive illness, and the action of amitriptyline.

The tyramine-dose/pressor response test was carried out on a series of patients suffering from primary depressive illness before and during treatment with amitriptyline. The severity of their depression was assessed during the study of the Hamilton Rating Scale (HRS). The decreased tyramine sensitivity induced by the drug, which is related to the inhibition of NA reuptake, correlated significantly with the plasma concentration of nortriptyline. However, contrary to the expectation of the noradrenaline hypothesis of depression, the decreased tyramine sensitivity, i.e., the degree of NA-reuptake blockade, did not show any correlation with clinical improvement following 6 weeks' treatment with amitriptyline.

Adult↗
PubMed1977

Effects on hypothalamic self-stimulation of drugs influencing dopaminergic neurotransmission injected into nucleus accumbens and corpus striatum of rats.

The role of the nucleus accumbens septi (ACB) and corpus striatum (CPU) in self-stimulation were investigated by injecting directly or indirectly acting stimulant drugs or a dopamine-(DA)-receptor blocking agent into each site bilaterally. d-Amphetamine (68 nmol) facilitated hypothalamic self-stimulation when injected into either side. Apomorphine (40 nmol) depressed or facilitated responding, the direction and magnitude of this effect being contingent (C = 0.52) on the effect of systemic injection (0.3 mg/kg.i.p.), and correlated with the difference between the effects of d- and l-amphetamine (0.5 mg/kg i.p.) but not with injection site. Haloperidol (6.6 nmol) in either site depressed self-stimulation. Tyramine (730 nmol), an agent believed to cause noncontingent displacement of transmitter from catecholamine terminals, depressed self-stimulation when injection into CPU, but facilitated it when injected into ACB. The site-specific effects found with tyramine but not with apomorphine may have been due to release by tyramine of transmitters other than DA.

Amphetamine↗
PubMed1978

Deprenyl administration in man: a selective monoamine oxidase B inhibitor without the 'cheese effect'.

After pretreatment with the selective monoamine oxidase B inhibitor, (-)-deprenyl, in doses sufficient for complete inhibition of the platelet enzyme, 4 normal and 6 parkinsoniam volunteers (2 receiving levodopa and 2 levodopa plus carbidopa) suffered no adverse pressor reaction ('cheese effect') after challenge with oral tyramine in amounts considerably greater than those likely to be encountered in a normal diet. Nor did the levodopa-deprenyl combination itself result in a pressor response. Normal human intestinal mucosa was shown predominantly to contain the deprenyl-insensitive A form of the enzyme, which presumably degraded administered tyramine in the deprenyl-treated volunteers; even those receiving the drug for prolonged periods manifested no 'cheese effect', suggesting that the A form remained uninhibited. Intestinal monoamine oxidase A was able to oxidise dopamine, whereas in human platelet or striatum the amine is a monoamine oxidase B substrate. Like tyramine, oral phenylethylamine challenge with amounts greater than those known to be present in a normal diet similarly gave rise to no adverse reaction in (-)-deprenyl-treated subjects; the reasons for this remain to be determined.

Adult↗
PubMed1981

Is the failure of (-)deprenyl, a selective monoamine oxidase B inhibitor, to alleviate depression related to freedom from the cheese effect?

The selective monoamine oxidase (MAO) B inhibitor (-)deprenyl failed to produce any greater benefit than placebo in a limited double-blind trial conducted in depressive patients. Its relative freedom from the so-called cheese effect was confirmed, however, in drug-treated patients challenged IV with tyramine. There is evidence to suggest that this cheese effect, a facilitated tyramine-induced hypertensive response, is pharmacologically distinct from MAO inhibition proper. Thus, it is conceivable that its central counterpart, an enhanced noradrenaline release due to the access of traces of tyramine to the CNS, is a prerequisite for any therapeutic benefit obtainable with the MAO-inhibitory drugs in general.

Blood Pressure↗
PubMed1986

Effects of adrenergic neurotransmitter on K transport in superfused segments of rat submaxillary gland.

The effect of the adrenergic neurotransmitter on K transport in the segments isolated from the rat submaxillary gland was investigated, employing the technique of electrical field stimulation (FS) and applying tyramine, a releasing drug for the catecholaminergic neurotransmitter. FS (16 Hz, 2 ms and 80 V for 1 min) caused a K release (peak value, 1.0 mumol/g/min) followed by a K uptake (peak value, 0.4 mumol/g/min) in the absence of any autonomic antagonist. Both FS-induced K release and uptake were blocked by the addition of tetrodotoxin (10(-7) g/ml). In the presence of atropine (1.4 X 10(-6) M), FS caused only a transient K uptake, which was abolished by the superimposed addition of propranolol (5 X 10(-6) M). Application of tyramine (6 X 10(-6)-6 X 10(-4) M) always only caused K uptake (peak value, 0.96 mumol/g/min), which was abolished by the addition of propranolol. The K uptake evoked either by FS or by tyramine application in the presence of atropine was not seen in the segments from rats pretreated (i.p.) with 6-hydroxydopamine. These results suggest that the adrenergic neurotransmitter activates mainly a beta-adrenergic receptor and evokes K uptake through receptor activation.

Adrenergic Fibers↗
PubMed1980

Differential effects of benztropine and desipramine on the high affinity uptake of paratyramine in slices of the caudate nucleus and hypothalamus.

The effect of benzotropine and desipramine on the uptake of dopamine and p-tyramine was studied in slices of caudate and hypothalamus. In the hypothalamus, of the various combinations of drugs and amines, desipramine inhibited p-tyramine uptake most effectively. In the caudate, benzotropine inhibited dopamine uptake most effectively. It is suggested that in the caudate, p-tyramine may possess its own unique transport system distinct from that utilized by dopamine which is inhibited by benzotropine.

Animals↗
PubMed1978

Absence of "cheese effect" during deprenyl therapy: some recent studies.

Although the selective monoamine oxidase (MAO) B inhibitor, (-)deprenyl, has been shown to be free from the "cheese effect" in man after tyramine challenge, the reason for this is far from clear: it may well be independent of the selective inhibitory action of the drug, for during chronic administration there is some evidence to suggest that both A and B forms of the enzyme are equally inhibited. By-passing the putative MAO A gut barrier in the pig (chosen because it possesses MAO B alone in all other tissues) by intravenous tyramine administration into the deprenyl-pretreated animal failed to provoke a pressor response, despite substantial MAO inhibition. Conversely, clorgyline (MAO A inhibitor) pretreatment, which resulted in minimal MAO inhibition, produced a profound hypertensive response, resembling that observed with the non-MAO-inhibiting drug, isoniazid. The most parsimonious explanation for these findings may be that two separate but closely associated pharmacological effects are normally found with "orthodox" MAO inhibitors, enzyme inhibition proper and facilitation of noradrenaline release from its binding sites during tyramine challenge.

Amphetamines↗
PubMed1997

5-Hydroxytryptamine and beta-adrenoceptors in rat isolated atria.

The positive chronotropic effect of a high concentration of 5-hydroxytryptamine (5-HT) in rat isolated atria results mainly from a tyramine-like mechanism and is linked to an increase in cAMP production by an indirect stimulation of beta-adrenoceptors. Using this preparation, we have compared the action of tyramine and 5-HT. The tyramine (0.15 microM)-induced increase in atrial rate was suppressed by atenolol (a beta 1-blocking drug) and by nadolol (a beta 1 beta 2-blocker), while the positive chronotropic effect of 5-HT was reduced by atenolol and suppressed by nadolol. The 5-HT-induced elevation in cAMP was unchanged in the presence of atenolol and abolished by nadolol. The involvement of beta 2-adrenoceptors in the effects of 5-HT could result from competition between 5-HT and noradrenaline at the beta 1-adrenoceptors that results in a fixation of noradrenaline on beta 2-adrenoceptors.

Adrenergic Agents↗
PubMed1980

Nicotine-induced release of noradrenaline from hypothalamic synaptosomes.

In order to elucidate the functional role of nicotinic receptors in the hypothalamus, the drug-induced release of noradrenaline from hypothalamic synaptosomes was studied utilizing [3H]noradrenaline ([3H]NA). The release of [3H]NA from synaptosomes was significantly increased with an increase of the dose of nicotine, carbamylcholine chloride, reserpine or tyramine hydrochloride added to the medium, whereas arecoline, atropine sulfate or mecamylamine hydrochloride had no significant effect. Mecamylamine hydrochloride completely inhibited the nicotine- or carbamylcholine-induced release of [3H] at the concentration of 10(-4) M, but had on effect on the reserpine- or tyramine-induced release of [3H]NA. A high concentration of potassium in the medium which depolarizes the synaptosome membrane significantly enhanced the release of [3H]NA. These results strongly suggest that there exist nicotinic cholinergic receptors in brain synaptic regions which play an important role in the function of hypothalamus by releasing noradrenaline and that the release mechanism of noradrenaline induced by nicotine is different from that induced by reserpine and tyramine. Although the existence of postsynaptic nicotinic receptor sites could not be reled out, the present studies indicate the importance of presynaptic cholinergic receptors in the brain.

Animals↗
PubMed1990

Excitation of rostral medullary pacemaker neurons with putative sympathoexcitatory function by cyclic AMP and beta-adrenoceptor agonists 'in vitro'.

This study explores the mechanism of action of catecholamines on rostral medullary pacemaker neurons with putative sympathoexcitatory function, in tissue slices. The firing rate of the pacemaker neurons of nucleus reticularis rostroventrolateralis (RVL pacemakers) was reversibly increased by agents which elevate intracellular levels of cAMP (forskolin and 8-br-cAMP). Forskolin dideoxy, an analog without action on adenylate cyclase, was ineffective and adenosine, a potential degradation product of 8-br cAMP produced inhibition exclusively and only in high doses (0.1-1 mM). The firing rate of these cells was uniformly increased by epinephrine and isoproterenol (10 microM) but unaffected by both phenylephrine (100 microM) and clonidine (up to 1 microM). These effects were abolished by pretreatment with the beta-adrenoceptor antagonist propranolol (10 microM) but they were unaffected by the alpha-antagonist phentolamine (100 microM). The indirectly-acting sympathomimetic amine tyramine (0.1-1 mM) activated all the cells tested. The effect of tyramine was antagonized by the beta-blocker pindolol and was absent 7 days after microinjection of the neurotoxin 6-hydroxydopamine into the lateral aspect of the RVL. Intracellular recordings indicated that both isoproterenol and tyramine enhanced the rate of depolarization of the pacemaker neurons during the interspike interval and produced a decrease in input resistance. After tetrodotoxin (TTX) pretreatment, isoproterenol produced a depolarization also associated with a reduction in input resistance. Three conclusions are proposed. First, RVL pacemakers have functional beta-adrenergic receptors whose activation increases their discharge rate via the intracellular production of cAMP. The effect of cAMP is due at least in part to the activation of an inward current which may be carried by a cation. Secondly, RVL neurons are in close proximity to a releasable pool of catecholamines which is susceptible to destruction by the cytotoxic agent 6-hydroxydopamine (6-OHDA). Finally it is tentatively suggested that the reduction in sympathetic tone produced by centrally acting beta-blockers could be due, at least in part, to an action of these agents on RVL pacemaker cells.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1990

Evidence that endogenous catecholamines are involved in alpha 2-adrenoceptor-mediated modulation of the aortic baroreceptor reflex in the nucleus tractus solitarii of the rat.

Microinjections of alpha-methylnoradrenaline and tyramine into the rat nucleus tractus solitarii (NTS) potentiated the depressor and bradycardiac responses to aortic nerve stimulation whereas yohimbine injected similarly inhibited them. NTS pretreatment with yohimbine inhibited the baroreflex potentiation effects of alpha-methylnoradrenaline and tyramine whereas intraventricular pretreatment with 6-hydroxydopamine inhibited only that of tyramine. These results provide evidence that endogenous catecholamines in the rat NTS are involved in alpha 2 adrenoceptor-mediated modulation of the aortic baroreceptor reflex.

Animals↗