Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

5-Hydroxytryptamine (5-HT) inhibited the incorporation of 14C from 14C-labelled glucose, pyruvate, citrate and acetate into fatty acids but it did not inhibit the conversion of 14C from citrate and acetate into CO2, and the citrate conversion into glyceride-glycerol in epididymal and mesenteric adipose tissue from 24h-fasted rats. 5-HT stimulated the formation of lactate from glucose and pyruvate, and increased the ratio of lactate produced/pyruvate taken up. This ratio was similar to the NADH:NAD ratio. These results indicate that 5-HT inhibits fatty acid synthesis in rat white adipose tissue by mechanisms similar to those of the catecholamines.
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PMID:Inhibitory effect of 5-hydroxytryptamine on lipogenesis in rat adipose tissues. 4 10

Effect of exogenous serotonin and blockade of its endogenous production on Angiotensin Converting Enzyme (ACE) in testes and epididymis was studied. Serotonin (30 mg/kg) and p-chlorophenylalanine (100 mg/kg) were injected for 4 and 3 days respectively. Serotonin reduced the weights of testes, seminal vesicle and ventral prostate whereas epididymal weight increased due to fluid accumulation. ACE was significantly reduced in tissue and fluid fractions of testes and epididymis of serotonin treated rats. pCPA had no effect on ACE levels. Serotonin seems to have direct effect on epididymis also.
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PMID:Changes in angiotensin converting enzyme in testes and epididymis of rat due to serotonin administration. 282 65

5-Hydroxytryptamine (5-HT) slightly inhibited the twitch contractions of rat vas deferens caused by single pulse field stimulation at 0.1 Hz. The inhibitory effect of 5-HT was much less in the epididymal portion than in the prostatic portion of the vas deferens. Ketanserin potentiated the prejunctional inhibitory effect of 5-HT and attenuated its stimulatory effect. This potentiation was observable only in the epididymal portion, of the vas deferens. Cyproheptadine and mianserin, but not methysergide, had essentially similar potentiating effects to those of ketanserin. These results suggest that the 5-HT receptor that mediates prejunctional inhibition is not of the 5-HT2 type, and that ketanserin acts by suppressing the 5-HT-induced stimulatory effect, which is possibly mediated by a postjunctional 5-HT2 receptor, thus unmasking the inhibitory effect of 5-HT.
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PMID:Ketanserin potentiates the prejunctional inhibitory effect of 5-hydroxytryptamine on rat vas deferens. 287 93

The application of bradykinin to the isolated, transmurally stimulated rat vas deferens caused two effects: increase of the basal tension of the tissue and potentiation of the magnitude of electrically driven twitches. These bradykinin responses were not evenly distributed along the ductus. The direct contractile action of bradykinin was found to be stronger in the epididymal half of the tissue while the potentiation of the muscle twitches was more pronounced in the prostatic half of the rat ductus. Bradykinin is more potent to potentiate the electrically driven twitches than to act as a postjunctional agonist. Tyr-bradykinin, [Tyr5]bradykinin and [Tyr8]bradykinin exhibited significant differences in the potency ratio to produce each of these responses. [Thi5,8,D-Phe7]bradykinin is a weak postjunctional agonist but was a full agonist to potentiate the electrically induced twitches. Furthermore, this compound antagonized the bradykinin-induced contractions. [Hyp3,Thi5,8,D-Phe7]bradykinin was devoid of agonist activity at either pre- or postjunctional sites; it behaved as a pure antagonist and was more than potent its non-hydroxylated analog. The addition of a D-Arg residue at the amino terminal increased the antagonist potency significantly. The pA2 of D-Arg-[Hyp3,Thi5,8,D-Phe7]bradykinin to antagonize the postjunctional effect of bradykinin was 6.35, a value that differed significantly from the value of 6.93 required to block the prejunctional effect of the peptide. The bradykinin receptor antagonists did not modify significantly the magnitude of the contractile responses caused by angiotensin II, norepinephrine or 5-hydroxy-tryptamine.
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PMID:Bradykinin receptor antagonists used to characterize the heterogeneity of bradykinin-induced responses in rat vas deferens. 289 46

The effect of age on the serotonin (5-HT)-induced prejunctional inhibition of twitch contractions induced in rat vas deferens by single-pulse field stimulation at 0.1 Hz was studied. The inhibitory effect of 5-HT gradually decreased with increasing age of the rats (4-15 weeks old) and was no longer detectable in preparations from rats over 15 weeks old. Moreover, on a further increase in age to 45 weeks, 5-HT conversely enhanced the twitch response of the vas deferens. The 5-HT2 antagonists ketanserin and mianserin potentiated the 5-HT-induced inhibition of contractions of the vas deferens of young rats (8-15 weeks old), and attenuated the amplifying effect of 5-HT on the responses of preparations from old rats (95 weeks old). Thus unmasking of the inhibition depended on the age of rats. This change occurred earlier in life in the prostatic portion of the vas deferens than in the epididymal portion. A functional decrease in 5-HT-mediated prejunctional inhibition and the resultant increase in amplification of the twitch response by 5-HT are probably responsible for the age-related decrease in prejunctional inhibition.
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PMID:Age-related change in serotonin-mediated prejunctional inhibition of rat vas deferens. 381 63

1 5-Hydroxytryptamine (5-HT) (5.16-1291 microM) produced a phasic contraction followed later by rhythmic contractions in the rat vas deferens, primarily in the epididymal half. 5-HT (129 microM) produced no response in Ca2+-free solution. Nifedipine (0.29 microM) or verapamil (2.04 microM) inhibited the initial phasic response to 5-HT, but inhibition of the rhythmic contractions required concentrations 5 fold (nifedipine) or 30 fold (verapamil) higher. 2 Methysergide (2.13 microM) abolished the phasic and reduced the frequency of the rhythmic contractions. Phentolamine (2.65 microM) did not affect the phasic response but reduced the amplitude of the rhythmic contractions. The combination of phentolamine (2.65 microM) and methysergide (2.13 microM) completely abolished the response to 5-HT (129 microM). 3 Desipramine (1.32 microM) had no effect on the phasic response to 5-HT (129 microM), but the rhythmic contractions were reduced in amplitude with no effect on their frequency. 4 In vasa deferentia removed from reserpine-treated or from guanethidine-denervated rats, both phasic and rhythmic components of the 5-HT (129 microM) contraction were augmented due to supersensitivity. 5 It is concluded that the phasic component of the 5-HT contraction is mediated by post-junctional 5-HT receptors, while the rhythmic component is mediated by the combination of post-junctional 5-HT receptors and noradrenaline released from neuronal stores. Assuming that nifedipine and verapamil are acting solely by inhibition of calcium channels, the phasic and rhythmic components of the 5-HT response may be mediated through separate Ca2+ channels. If this is correct, one channel might be a voltage-dependent channel and the other could be similar to, but distinct from the channel mediating the response to methoxamine.
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PMID:The contractile effects of 5-hydroxytryptamine on the rat isolated vas deferens. 715 Aug 68

The uptake of serotinin (5-hydroxytryptamine, 5-HT) by endothelial cells was studied in freshly isolated capillary and other microvessel (< 50 micrometers, inner diameter) endothelium obtained from rat epididymal fat pads. Endothelial cells incubated with [3H]-5-HT removed 60 pmol of [3H]-5-HT per mg of protein at 1 hr, an apparent Km of 3 X 10(-7) M and a Vmax of 20 pmol/mg of protein, measured at 15 min, were obtained. Uptake of 5-HT (10(-6) of M) was inhibited by ouabain, selected metabolic inhibitors (iodoacetate, 2--4 dinitrophenol and sodium azide), 4 degrees C, tryptamine (10(-5) M and the 5-HT antagonists, fluoxetine and imipramine (10(-5) M and 10(-4) M, respectively). At concentrations of 5-HT greater than Km value, uptake appears to be principally by nonfacilitative diffusion rather than by carrier-mediated transport.
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PMID:Serotonin uptake by isolated adipose capillary endothelium. 745 99

Some acute pharmacological effects have been examined of racemic ADT 16 (1,2,3,5,6,11b-hexahydro[1]benzothieno[3,2-g]indolizine hydrochloride), on peripheral and central responses mediated by 5-HT and adrenergic systems in the rat. In-vitro, ADT 16 (10-1000 nM), similarly to mianserin, antagonized the inhibitory responses to B-HT 920 of the electrically-stimulated rat isolated prostatic vas deferens. High concentrations of ADT 16 (10 microM), also resembled those of mianserin by potentiating twitch responses to electrical stimulation of the tissue. Contractile responses to phenylephrine of rat isolated epididymal vas deferens were antagonized by ADT 16 (0.3-1 microM). In the rat stomach fundus strip, ADT 16 (1-3 microM) antagonized contractions due to 5-HT. ADT 16 (0.1-1 microM) had no effect on responses to acetylcholine of the guinea-pig isolated ileum. In-vivo, in spinalized, decerebrated rats, fenfluramine- or clonidine-induced facilitation of flexor reflex activity of the anterior tibialis muscle was attenuated by ADT 16 (3 and 10 mg kg-1, i.v., and 3 mg kg-1, i.v. respectively). In the anaesthetized rat, L-3,4-dihydroxyphenylalanine (L-dopa)- or L-5-hydroxytryptophan (L-5-HTP)-induced increases in the frequency of spontaneous twitches of the anterior digastricus muscle were attenuated by ADT 16 (1 and 3 mg kg-1, i.v.; n = 4). It is concluded that ADT 16, similarly to mianserin, is a novel peripherally and centrally active antagonist of 5-HT and adrenergic responses in the rat.
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PMID:The action of 1,2,3,5,6,11b-hexahydro-[1]benzothieno [3,2-g]indolizine hydrochloride (ADT 16) on peripheral and central responses mediated by 5-hydroxytryptaminergic and adrenergic systems of the rat. 769 70

1. We have investigated the effects of methylenedioxymethamphetamine (MDMA, 'ecstasy') on peripheral noradrenergic neurotransmission in the rat. 2. In rat atrial slices pre-incubated with [3H]-noradrenaline and in the presence of desipramine (1 micronM) to prevent effects of MDMA on basal outflow of tritium, MDMA (10 micronM) significantly inhibited the release of tritium evoked by short trains of six pulses at 100 Hz every 10 s for 3 min. This effect did not occur in the presence of the alpha2-adrenoceptor antagonist yohimbine (1 micronM). 3. In epididymal portions of rat vas deferens in the presence of nifedipine (10 micronM), MDMA produced a concentration-dependent inhibition of single pulse nerve stimulation-evoked contractions with a pD2 of 5.88+/-0.16 (n=4). Inhibitory effects of MDMA were antagonized by the alpha2-adrenoceptor antagonist yohimbine (0.3 micronM), but not by the 5-hydroxytryptamine receptor antagonist cyanopindolol in a concentration (1 micronM) which markedly antagonized the inhibitory actions of the 5-HT-1 receptor agonist 5-carboxamidotryptamine. 4. In prostatic portions of rat vas deferens in the presence of cocaine (3 micronM), MDMA produced a concentration-dependent inhibition of single pulse nerve stimulation-evoked contractions with a pD2 of 5. 12+/-0.21 (n=4). In the absence of cocaine, only the highest concentration of MDMA (30 micronM) produced an inhibition, but the alpha2-adrenoceptor antagonist yohimbine (0.3 micronM) converted the response to MDMA from inhibition to potentiation of the stimulation-evoked contraction. 5. In radioligand binding studies, MDMA showed similar affinities for alpha2B, alpha2C and alpha2D-adrenoceptor sites, with pKi values of 5.14+/-0.16, 5.11+/-0. 05 and 5.31+/-0.14, respectively. 6 It is concluded that MDMA has significant alpha2-adrenoceptor agonist actions.
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PMID:Investigation of the prejunctional alpha2-adrenoceptor mediated actions of MDMA in rat atrium and vas deferens. 1055 34

The present study examined the density of 5-HT2A/2C receptors and 5-HT transporters in the brains of chronic high-fat diet-induced obese (cDIO) and obese-resistant (cDR) mice. Thirty-five male mice were used in this study. Twenty-eight mice were fed with a high-fat diet (40% of calories from fat) for 6 weeks and then classified as the cDIO (n=8) or cDR (n=8) mice according to the highest and lowest body weight gainers. Seven mice were placed on a low-fat diet (LF: 10% of calories from fat) and were used as controls. After 20 weeks of feeding, the sum of epididymal, perirenal, omental and inguinal fat masses was 9.3+/-0.3 g in the cDIO group versus 3.1+/-0.5 g in the cDR (p<0.005) and 1.5+/-0.1 g in the LF (p<0.001) groups. Using quantitative autoradiography techniques, the binding site densities of 5-HT2A/2C receptors and 5-HT transporters were measured in multiple brain sections of mice from the three groups. Most regions did not differ between groups but, importantly, the cDIO mice had a significantly higher 5-HT2A/2C binding density in the anterior olfactory nucleus and ventromedial hypothalamic nucleus (VMH) compared to the cDR and LF mice (+39% and +47%, p=0.003 and 0.045, respectively), whereas the latter two groups did not differ. The density of 5-HT2A/2C receptors in the VMH was associated with total amount of fat mass (r=0.617, p=0.032). On the other hand, the cDR mice had significantly lower 5-HT transporter binding than the cDIO and LF mice, respectively, in the nucleus accumbens (-44%, -38%, both p<0.02), central nucleus of the amygdaloid nucleus (-40%, -44%, p=0.003 and 0.009), and olfactory tubercle nucleus (-42%, -42%, both p=0.03). In conclusion, this study has demonstrated differentially regulated levels of the 5-HT2A/2C receptor and 5-HT transporter in specific brain regions of the cDIO and cDR mice. It provides neural anatomical bases by which genetic variability in 5-HT2A/2C receptors and 5-HT transporter may influence satiety and sensory aspects of energy balance.
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PMID:5-HT2A/2C receptor and 5-HT transporter densities in mice prone or resistant to chronic high-fat diet-induced obesity: a quantitative autoradiography study. 1527 82


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