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W Reimann

Publications and source records attributed to W Reimann.

At least 37 records · Page 2Linked to original sources
PubMed1989

Presynaptic alpha 2-adrenoceptors modulate the release of [3H]noradrenaline from rat spinal cord dorsal horn neurones.

Slices of the dorsal half of the rat spinal cord were used to investigate the existence of a noradrenergic feedback modulation of noradrenaline release. After crude preparation of the vertebral column, the spinal cord was ejected by hydraulic pressure and transverse slices were cut. These were preincubated with [3H]noradrenaline during 0.1 Hz electrical stimulation and then superfused and stimulated electrically for two periods. The stimulation-evoked release of [3H]noradrenaline was Ca2+-dependent and tetrodotoxin-sensitive. Pretreatment of the animals with the noradrenergic neurotoxin, DSP-4, reduced the tritium content in the slices and the stimulation-evoked release to less than 10% of the controls. Clonidine (0.01-1 microM) inhibited the evoked overflow by 60% maximally and yohimbine (0.1-1 microM) enhanced it by 160% maximally. The effects of clonidine were antagonized by yohimbine. These results provide evidence that noradrenaline release from spinal cord slices is controlled by an alpha 2-adrenoceptor-mediated, negative feedback mechanism.

Animals↗
PubMed1988

W-7 at calmodulin-antagonistic concentrations facilitates noradrenaline release from rat brain cortex slices.

Slices from rat brain occipital cortex were preincubated with [3H]noradrenaline then superfused and stimulated electrically. W-7, 10 mumol/l, enhanced the stimulation-evoked overlow. Binding experiments with W-7 evidenced weak displacement of [3H]yohimbine and no displacement of [3H]prazosin. Release experiments with the addition of clonidine, cocaine or phentolamine provided no evidence for major interference of W-7 with alpha-adrenergic or uptake mechanisms. Facilitation could have been due to inhibition of a calmodulin-dependent enzyme which could not be identified from the present results.

Animals↗
PubMed1988

Voltage-sensitive Ca2+ channels in rat brain neocortical noradrenergic nerve terminals. Different sensitivity to inorganic and organic Ca2+ channel antagonists.

In rat cerebral cortex slices we investigated the Ca2+ dependency of noradrenaline release and the influence of inorganic and organic Ca2+ antagonists. Slices were preincubated with 3H-noradrenaline and then superfused with noradrenaline-free medium. Release of 3H-noradrenaline was elicited by electrical pulses. The stimulation-evoked release was dependent on the external Ca2+ concentration and was inhibited by Cd2+, Co2+ and Mg2+ in a concentration-related manner. These results indicate that electrically stimulated noradrenaline release depends on the Ca2+ influx after opening of voltage-sensitive Ca2+ channels. Organic Ca2+ antagonists were used in concentrations which had no major influence on the basal release rate. Of the drugs tested (bepridil, diltiazem, flunarizine, nimodipine, isradipine, prenylamine, verapamil) only flunarizine and nimodipine showed a minor inhibition of the stimulation-evoked release, which was less than 20% at 1 mumol/l. With nimodipine 10 mumol/l, there was a 6% facilitation of release. All other drugs except flunarizine and verapamil caused a slight facilitation of the stimulation-evoked release. The results provide evidence that the organic Ca2+ channel antagonists investigated do not or only minimally interfere with the noradrenergic nerve terminal Ca2+ channels in a tissue slice preparation. The release-facilitating effects of most organic Ca2+ antagonists cannot be interpreted by the present results.

Animals↗
PubMed1985

Gabapentin decreases monoamine release without affecting acetylcholine release in the brain.

Superfused rat brain cortex slices preincubated with 3H-noradrenaline or 3H-serotonin and superfused rabbit caudate nucleus slices preincubated with 3H-choline were used to examine the effects of gabapentin (an amino acid chemically related to gamma-aminobutyric acid, GABA) on the electrically evoked 3H overflow. Gabapentin inhibited the electrically (3 Hz) evoked 3H overflow from slices preincubated with the 3H-monoamines in a concentration-dependent manner (at 1 mmol/l by 20-30%), but did not affect the evoked overflow from slices preincubated with 3H-choline. The following drugs did not modify the inhibitory effects of gabapentin: bicuculline, RS-baclofen, GABA, phentolamine, metitepin, cocaine, and the inhibitor of serotonin uptake, 6-nitroquipazine. Gabapentin did not modify the inhibitory effect of GABA on the evoked 3H overflow from slices preincubated with 3H-serotonin. In slices preincubated with 3H-noradrenaline the inhibitory effect of gabapentin was still observed when the stimulation frequency was 10 instead of 3 Hz. In conclusion, gabapentin mimics GABAB receptor activation, but it appears to act by a GABA receptor-independent, as yet unidentified mechanism.

Acetates↗
PubMed1984

Evidence for neuronal uptake and release of norfenefrine and evaluation of its alpha-agonistic effects in the rabbit pulmonary artery.

Rabbit pulmonary artery strips were used for the evaluation of the alpha 1-/alpha 2-agonistic activity of norfenefrine (active principle of the antihypotensive agent Novadral) and for the investigation of neuronal uptake and release mechanisms for norfenefrine in the vessel wall. At 0.1 and 1 mumol/l, norfenefrine caused contractions of the artery strips, while presynaptic inhibition of stimulation-evoked noradrenaline release could not be detected with certainty. Thus, in the range tested, alpha 1-agonistic activity was more pronounced. Uptake and release of 3H-norfenefrine was studied on noradrenaline-depleted arteries. Rabbits were pretreated either with alpha-methyl-p-tyrosine (metirosine, alpha-MT) to inhibit noradrenaline synthesis without affecting storage vesicle function or with reserpine to eliminate vesicular storage capacity. In arteries from animals pretreated with alpha-MT, more substance was retained after preincubation with 3H-norfenefrine, in comparison with reserpine pretreated arteries, and about 2% of the substance was released from Arteries from reserpine pretreated animals retained less 3H-norfenefrine after preincubation, in comparison with alpha-MT pretreated arteries, and less than 0.2% was released per stimulation period. After alpha-MT treatment, tension developed upon stimulation was enhanced after norfenefrine preincubation, while contractions of reserpine pretreated arteries were independent of norfenefrine preincubation. These results provide evidence for an uptake of norfenefrine in the noradrenaline storage vesiculation period. After alpha-MT treatment, tension developed upon stimulation was enhanced after norfenefrine preincubation, while contractions of reserpine pretreated arteries were independent of norfenefrine preincubation. These results provide evidence for an uptake of norfenefrine in the noradrenaline storage vesicles and a vesicular co-secretion of norfenefrine with noradrenaline upon stimulation. The impaired sympathetic transmission was thereby improved.

2-Hydroxyphenethylamine↗
PubMed1983

Inhibition by GABA, baclofen and gabapentin of dopamine release from rabbit caudate nucleus: are there common or different sites of action?

Slices of rabbit caudate nucleus were preincubated with [3H]dopamine then superfused and stimulated electrically. Baclofen, GABA and gabapentin 10(-4) and 10(-3) mol/l reduced the stimulation-evoked overflow of tritium in a similar manner. The effects of the substances were reinvestigated while one of them was present in a high concentration throughout the superfusion. These interaction experiments showed that baclofen and GABA have a common presynaptic site of action which is different from that of gabapentin.

Acetates↗
PubMed1982

alpha-Adrenoceptor-mediated inhibition of noradrenaline release in rabbit brain cortex slices. Receptor properties and role of the biophase concentration of noradrenaline.

Brain cortex slices from rabbits were preincubated with [3H]noradrenaline and then superfused and stimulated electrically at 3Hz. In the presence of cocaine 30 microM, unlabelled noradrenaline, alpha-methylnoradrenaline, clonidine, oxymetazoline, xylazine and guanabenz decreased, whereas yohimbine, corynanthine, phentolamine, tolazoline and azapetine increased the stimulation-evoked overflow of tritium. Phenylephrine and prazosin had no effect on the evoked overflow except at concentrations that greatly accelerated the basal outflow of tritium. The results indicate that the noradrenergic axons of rabbit brain cortex are endowed with presynaptic alpha-adrenoceptors which are exclusively of the alpha 2-type. Addition of various concentrations of cocaine, addition of pargyline, or stimulation at different current strengths was used to obtain either a high or low stimulation-evoked overflow of tritium. Independently of the method used, a low evoked overflow coincided with a large percentage inhibition produced by 0.1 micro M clonidine, whereas a high evoked overflow coincided with a smaller percentage inhibition produced by clonidine. The results indicate that drugs which block the re-uptake of noradrenaline diminish the presynaptic inhibitory effect of alpha-adrenergic agonists by increasing the biophase concentration of released noradrenaline.

Adrenergic alpha-Agonists↗
PubMed1982

Are presynaptic dopamine autoreceptors and postsynaptic dopamine receptors in the rabbit caudate nucleus pharmacologically different?

Slices of the rabbit caudate nucleus were preincubated with [3H]dopamine or [3H]choline and then superfused and stimulated electrically. Apomorphine reduced the stimulation-evoked overflow of tritium over the same concentration range, independently of whether slices had been pre-incubated with [3H]dopamine or with [3H]choline. Each of three antagonists--molindone, sulpiride and metoclopramide--increased the evoked overflow of tritium over the same concentration range in experiments with [3H]dopamine and those with [3H]choline. For each antagonist, the pA2 values against apomorphine obtained in [3H]dopamine experiments and in [3H]choline experiments were very similar. This study is a functional in vitro approach to receptor characterization, as opposed to radioligand binding studies or in vivo investigations. The results show that the dopamine receptor agonist apomorphine and three antagonists are unable to distinguish between the presynaptic, release-inhibiting dopamine autoreceptors and those postsynaptic dopamine receptors which, when activated, depress the release of acetylcholine. Although there are certainly more dopamine receptors in the caudate nucleus, these two physiologically important groups seem to be closely related.

Acetylcholine↗
PubMed1982

On the mechanism of the vasopressin-induced inhibition of renin release.

The isoprenaline-induced renin release was used to study both in vivo and in vitro and mechanism of the inhibitory effect of vasopressin on renin secretion. (1) The vasopressin analogue [1-deaminopenicillamine, 2-(0-methyl)-tyrosine]-arginine-vasopressin, which antagonizes the vasopressor response to vasopressin but possesses antidiuretic potency, abated the increase in plasma renin concentration following isoprenaline injection in the conscious rat without altering the fall in arterial blood pressure, (2) In a continuous superfusion system of rat kidney cortical slices, vasopressin in concentrations up to 10(-6) M failed to affect the isoprenaline-induced increase in renin secretion, which was evidently beta-adrenoceptor-mediated. In contrast, angiotensin II (10(-6) M) prevented the renin release in response to isoprenaline. These results led us to conclude that the inhibition of renin release caused by vasopressin is not necessarily related to its vasoconstrictor potency. The mechanism, through which vasopressin works, appears to differ from that of angiotensin II and is non functional in renal cortical slices.

Animals↗
PubMed1982

Gamma-aminobutyric acid can both inhibit and facilitate dopamine release in the caudate nucleus of the rabbit.

Slices from rabbit caudate nucleus were preincubated with [3H]dopamine and then superfused and stimulated electrically. gamma-Aminobutyric acid (10-4) and 10(-3) mol/L increased both the basal and the stimulation-evoked overflow of tritium. The effects were not changed by picrotoxin and were only slightly reduced by bicuculline. In the presence of nipecotate 10(-3) mol/L, gamma-aminobutyric acid decreased rather than enhanced the basal and the evoked overflow. The inhibition persisted in the presence of bicuculline. Muscimol did not affect, whereas baclofen decreased, the evoked overflow of tritium. Similar results obtained with synaptosomes that were stimulated by 30 mmol/L K+. The results indicate that gamma-aminobutyric acid can both facilitate and depress the release of dopamine. Facilitation occurs after entry of gamma-aminobutyric acid into the dopaminergic terminal axons, whereas inhibition if probably mediated by a receptor site located in the membrane of these terminals.

Animals↗
PubMed1981

Effect of prostaglandins D2, E2 and F2alpha on catecholamine release from slices of rat and rabbit brain.

Slices of rabbit or rat brain cortex were preincubated with [3H]noradrenaline, and slices of rabbit caudate nucleus or rat stratum with [3H]dopamine. The slices were then superfused and stimulated electrically. In rat cortex slices, PGE2 (0.01-1 millimicronmol/l) markedly reduced the stimulation-evoked overflow of tritium. PGF2alpha (1 millimicronmol/l) caused a slight decrease only after the formation of endogenous prostaglandins had been blocked by indomethacin. PGD2 (1 millimicronmol/l) had no effect. In slices of rabbit cortex and caudate nucleus as well as in rat striatal slices, none of the prostaglandins (1 millimicronmol/l) caused any change, irrespective of whether the production of endogenous prostaglandins was intact or blocked. The results show that, of three major prostaglandins that occur in the brain, only PGE2 is a potent presynaptic inhibitor of noradrenaline release in the rat. The catecholamine neurones of rabbit brain, and the dopamine neurones of rat striatum, are resistant to these prostaglandins.

Animals↗