Disease relevance of sulpiride

• Treatment of duodenal ulcer with antacid and sulpiride. A double-blind controlled study [1].
• Tiapride and sulpiride in Parkinson's disease [2].
• Sulpiride (SUL, 20 mg kg-1 day-1) induces weight gain, hyperphagia, hyperprolactinemia, hypogonadism, and perhaps increased insulin sensitivity in rats [3].
• Antipsychotic drug-induced obesity in rats: correlation between leptin, insulin and body weight during sulpiride treatment [3].
• On day 15, weight gain was significantly greater in the infants whose mothers received sulpiride, but later, no differences were detectable between groups of infants despite the disparity in PRL levels in their mothers [4].

Psychiatry related information on sulpiride

• The effect on cataplexy was stereospecific for the S(-) enantiomer of sulpiride (a D2 antagonist) and the R(+) enantiomer of 3-PPP (a D2 agonist) [5].
• In experiment 1, microinjections of the D1 antagonist SCH-23390 (0.05, 0.5, or 5 microg/&microl), but not the D2 antagonist sulpiride (0.05, 0.5, or 5 microg/microl), into the prelimbic region of the PFC before the test phase disrupted performance of the delayed task without affecting response latencies [6].
• Prolactin response to sulpiride before and after sleep deprivation in depression [7].
• Sulpiride (and other D2/D3 antagonists) may therefore be an attractive new therapeutic indication in human narcolepsy [8].
• Neuroleptics in the short-term treatment of anorexia nervosa. A double-blind placebo-controlled study with sulpiride [9].

High impact information on sulpiride

• In addition to E2, the proliferation of cancer cells, assessed by the measurement of thymidine labeling indices (TLIs), was demonstrated to be enhanced by ovine prolactin (oPRL) and Sulpiride and strongly slowed down by castration and 2-bromo-alpha-ergokryptin treatment, thus emphasizing the great importance of PRL in mammary cancer development [10].
• This inhibition was blocked by D2 receptor blockade with metoclopramide or sulpiride, but not by D1 receptor blockade [11].
• Inhibition of gastrin secretion by sulpiride treatment in duodenal ulcer patients [12].
• Quinpirole increased DAT activity that was blocked by sulpiride and the protein kinase A selective inhibitor H-89 [13].
• The effects of DA and amphetamine were attenuated by the D1 receptor antagonist SCH23390 but not by the D2 receptor antagonist sulpiride [14].

Chemical compound and disease context of sulpiride

• The effect of aluminum-magnesium hydroxide tablets (800 mg seven times per day) and that of sulpiride, a hypothalamic neurolaptic, were studied in 101 patients with duodenal ulcer in a double-blind controlled 4-wk trial [1].
• In a double blind study, 35 patients with duodenal ulcer diagnosed by endoscopy were randomly assigned to receive cimetidine 800 mg daily and 38 patients to receive cimetidine 800 mg plus sulpiride 200 mg daily [15].
• Alteration of feedback mechanism of estrogen on gonadotropin by sulpiride-induced hyperprolactinemia [16].
• Clinical and endocrinological analyses of patients with galactorrhea and menstrual disorders due to sulpiride or metoclopramide [17].
• Effect of sulpiride-induced hyperprolactinemia on serum testosterone response to HCG in normal men [18].

Biological context of sulpiride

• We investigated the effects of dopaminergic drug treatment (sulpiride) on the relationship between somatosensory stimulus intensity and cortical response measured electrophysiologically by somatosensory-evoked potentials (SEP) and functional magnetic resonance imaging (fMRI) [19].
• Augmentation of puerperal lactation by oral administration of sulpiride [20].
• After 6 months of levosulpiride therapy, the time of gastric emptying was significantly reduced from 321 +/- 14 to 261 +/- 9 min (P < 0.001) and dyspeptic symptoms had improved [21].
• The mean (+/-SE) total milk yield during the first 5 postpartum days in the sulpiride group (1211.7 +/- 65.0 ml) was significantly greater than that in the control group (916.0 +/- 66.0 ml) [20].
• (-) Sulpiride reversibly blocked the dopamine-induced current with IC50 values of 5, 300, and 2000 nM for D2, D3, and D4 receptors, respectively [22].

Anatomical context of sulpiride

• In short, we have demonstrated enhanced functional and effective connectivity of human caudate nucleus following sulpiride treatment, which is compatible both with the anatomy of ascending dopaminergic projections and with electrophysiological studies indicating abnormal coherent oscillations of CST neurons in parkinsonian states [23].
• The more salient effect of sulpiride was to increase functional connectivity between caudate and both thalamus and ventral midbrain [23].
• The local application of (-)sulpiride, 200 ng side-1, into the nucleus accumbens produced a suppression of conditioned avoidance behavior in male rats, 10 and 90 min after injection [24].
• The local application of (-)sulpiride into the posterior neostriatum, or into the prefrontal cortex, produced no statistically significant effect on conditioned avoidance behavior 10 or 90 min after injection [24].
• These data demonstrate that administration of LHRH agonist can inhibit the hyperprolactinemic effect of sulpiride, suggesting a direct action of the analog on the pituitary gland to modulate PRL secretion [25].

Associations of sulpiride with other chemical compounds

• DA1 antagonists (SKF83566 and SCH23390), but not DA2-antagonist (sulpiride), blocked dopamine inhibition [26].
• In the absence but not presence of doxycycline, a 49% reduction in pituitary growth and 58% reduction in the increase of circulating prolactin levels were observed in estrogen, but not estrogen/sulpiride, treated rats [27].
• No induction of 2D4 was observed with the dopamine D2 receptor blockers haloperidol, chlorpromazine, and sulpiride or with the serotonin receptor blocker mianserin [28].
• Remitted schizophrenic outpatients were prophylactically treated to prevent relapse with three different doses of timiperone or sulpiride for a year in a double-blind controlled study employing a randomized design [29].
• By comparing the dose-response curves of four drugs tested in the same fashion, haloperidol and sulpiride were superior to propericiazine and timiperone because they displayed a wider dose range for the maintenance treatment of remitted schizophrenic outpatients [29].

Gene context of sulpiride

• Conversely, an iv bolus of sulpiride (25 mg), a dopaminergic antagonist, given to four subjects after 240 min, brought about a marked increase in serum PRL values above the plateau level [30].
• Although the DAR2 antagonist, sulpiride, reversed BIM-23A387-induced GH suppression, blockade of SSTR2 by the selective SSTR antagonist, BIM-23454, did not block BIM-23A387-suppressed GH secretion [31].
• LIF (5 nM) also suppressed PRL levels in primary rat pituitary cultures by 70% (P < 0.005), and in rat MMQ pituitary tumor cells, and this effect was also reversed by sulpiride (200 micro M) [32].
• The same dose of 5HTP resulted in a significant further increase in plasma PRL exceeding the levels elevated by sulpiride injections in NRS-treated rats [33].
• Three compounds showed better activity against hCA VB over hCA II, among which were sulpiride and ethoxzolamide, which were 2 times more effective inhibitors of the mitochondrial over the cytosolic isozyme. hCA VB is a druggable target and some of its inhibitors may lead to the development of novel antiobesity therapies [34].

Analytical, diagnostic and therapeutic context of sulpiride

• Self-administration could be attenuated by including equimolar concentrations of the dopaminergic D2-receptor antagonist sulpiride in the microinjection system [35].
• Iontophoretic application of sulpiride, a selective D2 antagonist, onto the HIPP-ACC terminals attenuated the increased terminal excitability of these neurons produced by conditioning VTA stimulation, while intraperitoneal injection of SCH23390, a selective D1 antagonist, failed to attenuate this effect [36].
• Results indicate that sulpiride has comparable effects on power law parameters estimated from SEP and fMRI, but fMRI has superior sensitivity to detect drug effects on somatosensory cortical recruitment by graded stimulation [19].
• We have used sulpiride- and oestrogen-induced lactotroph hyperplasia within the rat AP gland as an in vivo animal model [37].
• The concentration of DA released during the second pulse of a train was 58% of that released by the first pulse, an effect that is partially blocked by the addition of 2 microM sulpiride, a D2 antagonist, to the perfusion buffer [38].

References