Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P46098 (5-HT3 receptor)
2,290 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The cardiovascular effects of the 5-HT2 antagonist ICI 169,369 have been investigated in pentobarbitone anaesthetized rats and in pithed rats whose blood pressure was supported by a vasopressin infusion. 2. In anaesthetized rats, cumulative doses (0.1-3.0 mg kg-1) of ICI 169,369 caused dose-related large transient falls in heart rate and blood pressure followed by a slow dose-related decline in both parameters. 3. Pretreatment with atropine methonitrate (1 mg kg-1) alone or in combination with atenolol (1 mg kg-1) or bi-vagotomy blocked the transient changes in blood pressure and heart rate caused by ICI 169,369. The long-term fall in heart rate was also attenuated by either atropine or atenolol; however, the combination of atenolol and atropine was more effective. None of the above pretreatments affected the long-term fall in blood pressure caused by ICI 169,369. 4. The cardiovascular effects of ICI 169,369 were unaffected by pretreatment with MDL 72222 (1 mg kg-1) and failed to show cross-tachyphylaxis with phenylbiguanide. 5. In pithed rats whose blood pressure was maintained with vasopressin, ICI 169,369 failed to cause any of the above transient and long-term effects on blood pressure and heart rate. 6. The study indicates that ICI 169,369 is capable of stimulating cardiopulmonary afferents through a non 5-HT3 receptor mechanism and has a central hypotensive action.
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PMID:Evidence suggesting that the 5-HT2 antagonist ICI 169,369 activates vagal afferents and in addition has a central hypotensive action in anaesthetized rats. 209 95

Arginine8-vasopressin (AVP) has been shown repeatedly to affect learning and memory and to maintain tolerance to ethanol if the brain serotonin and catecholamine systems are intact. In the present study, 5,7-dihydroxytryptamine (5,7-DHT) was injected intracerebroventricularly to disrupt serotonergic projections from the raphe to the forebrain. This resulted in a marked decrease in 5-hydroxytryptamine (5-HT) immunoreactivity in the terminal areas of the septum and the hippocampus, but not in the serotonin-containing neuronal cell bodies in the raphe nuclei. In control rats, tolerance to the motor-impairing effects of ethanol lasted for only 5 days after the cessation of ethanol treatment but could be maintained indefinitely for as long as AVP was given. In the 5,7-dihydroxytryptamine-lesioned rats, AVP was unable to maintain the tolerance. Continuous intracerebroventricular infusion of 5-HT restored the ability of AVP to maintain ethanol tolerance in the lesioned rats. A selective 5-HT2 agonist (alpha-methylserotonin) was equally effective, and a 5-HT3 receptor agonist (2-methylserotonin) was slightly less effective, but the 5-HT1A agonist dipropylaminotetralin (8-hydroxy-dipropylaminotetralin) was totally ineffective in this respect. The results indicate selective involvement of brain 5-HT2 and possibly 5-HT3 receptors in mediating AVP maintenance of tolerance to ethanol but do not pinpoint their specific loci or roles.
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PMID:Selective involvement of central 5-HT2 receptors in the maintenance of tolerance to ethanol by arginine8-vasopressin. 807 72

The neurotransmitter serotonin (5-HT) stimulates the secretion of vasopressin and oxytocin, and 5-HT is involved in the mediation of the vasopressin and oxytocin response to stress. In male Wistar rats, we investigated the 5-HT receptors involved in the 5-HT-induced increase of mRNA expression of vasopressin and oxytocin in the hypothalamic paraventricular nucleus (PVN) and supraoptic nucleus (SON). The 5-HT precursor, 5-hydroxytryptophan, injected in combination with the 5-HT reuptake inhibitor, fluoxetine, increased oxytocin mRNA expression in the PVN, and the concentration of vasopressin and oxytocin in plasma, whereas mRNA in the SON was not affected. Intracerebroventricular infusion of 5-HT agonists selective for the 5-HT1A, 5-HT1B, 5-HT2A and 5-HT2C receptor increased oxytocin mRNA in the SON and PVN. Infusion of agonists selective for the 5-HT2A + 2C receptor increased vasopressin mRNA in the PVN, whereas none of the 5-HT agonists affected vasopressin mRNA in the SON. All the 5-HT agonists infused increased peripheral oxytocin concentration and vasopressin was increased by stimulation of the 5-HT2A, 5-HT2C and 5-HT3 receptor. Intracerebroventricular infusion of 100 nmol 5-HT increased the extracellular hypothalamic concentration of vasopressin as measured by microdialysis in the PVN. To evaluate the involvement of hypothalamic-pituitary system in the 5-hydroxytryptophan and fluoxetine-induced vasopressin secretion, rats were immunoneutralized with a specific anti-corticotropin-releasing hormone antiserum. This treatment reduced plasma vasopressin and oxytocin responses. We conclude that stimulation with 5-hydroxytryptophan or 5-HT agonists increases mRNA expression of oxytocin in the PVN and the SON via stimulation of at least 5-HT1A, 5-HT1B, 5-HT2A and 5-HT2C receptors. Vasopressin mRNA in the PVN was increased only via the 5-HT2 receptor, whereas vasopressin mRNA in the SON does not seem to be affected by 5-HT stimulation. Corticotropin-releasing hormone appears to be partly involved in the mediation of 5-HT induced vasopressin and oxytocin secretion.
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PMID:Serotonin stimulates hypothalamic mRNA expression and local release of neurohypophysial peptides. 1271 7