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K Racké

Publications and source records attributed to K Racké.

97 records · Page 6Linked to original sources
PubMed1983

A comparison of the release of endogenous dopamine from the neural and the intermediate lobe of the rat hypophysis after electrical stimulation of the stalk.

Dopamine (DA) was released from the isolated neural lobe of the pituitary gland by electrical stimulation of the pituitary stalk. This observation completes the evidence for DA to be classified as a neurotransmitter substance in the neural lobe in the rat hypophysis. From the experiments on the isolated neural lobe and simultaneous experiments on the combined neuro-intermediate lobe it could be calculated that the DA release from the intermediate lobe was about three times larger than that from the neural lobe. Electrical stimulation of the pituitary stalk in the presence of pargyline and TEA led to an increase in DA synthesis in the neural lobe. This effect did not occur in the intermediate lobe.

Animals↗
PubMed1982

Isoprenaline and forskolin increase evoked vasopressin release from rat pituitary.

Isolated neurointermediate lobes of rat pituitaries were incubated in Krebs solution. The vasopressin release evoked by electrical stimulation (0.2 ms, 80 V, 15 Hz, 10 s trains at 10 s intervals for a total of 10 min) was completely inhibited by tetrodotoxin. Isoprenaline increased the evoked vasopressin release to a maximum of 60% (EC50 10 nM) and this effect was antagonized surmountably by propranolol. Forskolin increased the vasopressin release by 98%. These results suggest the presence within the neurohypophysis of a beta-adrenoceptor-linked adenylate cyclase facilitating vasopressin secretion.

Animals↗
PubMedDate not supplied

Nicotinic and muscarinic modulation of 5-hydroxytryptamine (5-HT) release from porcine and canine small intestine.

Strips of porcine and canine small intestine were incubated in vitro and the release of 5-hydroxytryptamine (5-HT) was determined by HPLC with electrochemical detection. The spontaneous outflow of 5-HT from the porcine and canine small intestine largely reflects calcium-dependent 5-HT secretion from enterochromaffin cells which are under a spontaneous neuronal, excitatory input as indicated by the inhibitory effect (30-40%) of tetrodotoxin. In both species, nicotine enhanced the release of 5-HT in a concentration-dependent manner by a maximum of about 50% at 100 microM. This effect was blocked by the nicotine receptor antagonist hexamethonium, but not by the subtype-selective nicotine receptor antagonist alpha-bungarotoxin. The effect of nicotine was rapidly desensitized. The presence of tetrodotoxin abolished the effect of nicotine on 5-HT release in canine tissue but not in porcine tissue. The presence of the muscarine receptor antagonist scopolamine prevented the effect of nicotine on 5-HT release from canine tissue, but significantly enhanced 5-HT release from porcine tissue. The muscarine receptor agonist oxotremorine inhibited 5-HT release from porcine tissue, but increased 5-HT release from canine tissue. However, in the presence of tetrodotoxin, oxotremorine enhanced 5-HT release in tissue from both species. In conclusion, activation of nicotine receptors induce the release of 5-HT from porcine and canine small intestine. In the dog, the effect of nicotine is mediated via the release of acetylcholine which then stimulates 5-HT release via muscarine receptors on the enterochromaffin cells. In the pig, the stimulatory effect of nicotine appears to be located directly on the enterochromaffin cells. In addition, activation of neuronal muscarine receptors in the porcine small intestine induced the release of a previously unidentified neurotransmitter which inhibited 5-HT release. Nicotine, via cholinergic interneurons, also appears to induce the release of this inhibitory neurotransmitter which opposes the direct stimulatory action of nicotine on 5-HT release.

Acetylcholine↗
PubMedDate not supplied

Effects of cigarette smoking or ingestion of nicotine on platelet 5-hydroxytryptamine (5-HT) levels in smokers and non-smokers.

Platelets of healthy smokers and non-smokers were prepared and their content of 5-hydroxytryptamine was determined by HPLC with electrochemical detection. Platelet 5-HT levels in smokers (728 +/- 156 pmol per 10(8) platelets, mean +/- SEM, n = 9) were significantly higher than those in non-smokers (353 +/- 156 pmol per 10(8) platelets, n = 11). Smoking of a single cigarette caused a transient increase in platelet 5-HT levels by about 350% in non-smokers, but had no additional effect in smokers. Similarly, chewing of nicotine gum (4-8 mg nicotine) resulted in a transient increase in platelet 5-HT by about 100% in non-smokers, but not in smokers. In conclusion, smoking of cigarettes can cause an increase in platelet 5-HT, most likely via an enhanced supply of 5-HT from enterochromaffin cells which can be stimulated via nicotine receptors.

Administration, Oral↗
PubMedDate not supplied

Effects of the benzodiazepine receptor agonist midazolam and antagonist flumazenil on 5-hydroxytryptamine release from guinea-pig intestine in vitro. Indirect support for a "natural" benzodiazepine-like substance in the intestine.

Isolated segments of the guinea-pig small intestine and the guinea-pig stomach were vascularly perfused and the release of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid into the portal venous effluent determined by high pressure liquid chromatography with electrochemical detection. Test substances were applied intraarterially. The benzodiazepine receptor agonist, midazolam, concentration-dependently increased (by 58%, at 1 nmol/l) and decreased (by 32%, at 100 nmol/l) the release of 5-HT from small intestine preparations. Both effects were blocked by the benzodiazepine receptor antagonist flumazenil (10 nmol/l) The stimulatory effect of midazolam was also abolished in the presence of tetrodotoxin (1 mumol/l) or scopolamine (100 nmol/l). In the absence of tetrodotoxin, flumazenil (10 nmol/l) alone decreased the release of 5-HT from the small intestine by 41%, but it increased the release of 5-HT by 50% in the presence of tetrodotoxin. Both effects of flumazenil were abolished in the presence of bicuculline (50 mumol/l). In the absence of tetrodotoxin, flumazenil (10 nmol/l) decreased also the release of 5-HT and its metabolite from the perfused stomach by about 40%, whereas midazolam (1 nmol/l) caused an increase by about 60%. In conclusion, benzodiazepine receptors modulate the previously described intrinsic GABAergic regulation of 5-HT release from enterochromaffin cells in the guinea-pig intestine. It is suggested that an endogenous benzodiazepine-like substance of non-neuronal origin is present in the small intestine and stomach of the guinea-pig.

Animals↗