Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A modification of the rat isolated seminal vesicle preparation is described, emphasizing the necessity to use younger animals (40-50 days old and weighing between 125 and 150 g) and to expel thoroughly all vesicular contents. Under the experimental conditions used (tissues suspended under a resting tension of 350 mg in a continuous flow of a modified Krebs solution run at the rate of 15 ml/min, maintained at 32 degrees C, and bubbled with 5% CO2 in O2), the preparation was quite sensitive, but only to a few selected agonists, and remained viable for over 4-6 hr. Adrenaline, noradrenaline, dopamine, and acetylcholine all produced concentration-dependent and reproducible contractions. However, histaminergic, serotoninergic, purinergic, and opioid agonists were inactive as were prostaglandins of the E and F series and the polypeptides angiotensin, vasopressin, and oxytocin. In general, the tissue was rather insensitive to relaxant drugs, with only papaverine and sodium nitrite producing some relaxation in tissues previously contracted by carbachol. Advantages of the preparation include marked responsiveness, but only to a few selected agonists, and suitability for use as a paired tissue. It is suggested that employed under suitable experimental conditions, the preparation deserves a more frequent consideration for use during pharmacological investigations concerned with postsynaptic aspects of noradrenergic or cholinergic transmission.
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PMID:Pharmacological evaluation of the isolated rat seminal vesicle preparation. 395 Dec 38

Vasopressin and oxytocin exert pronounced effects on behavior by a direct action on the brain. A single injection of vasopressin results in a long-term inhibition of extinction of a conditioned avoidance response suggesting that vasopressin triggers a long-term effect on the maintenance of a learned response, probably by facilitation of memory processes. In addition vasopressin improves passive avoidance behavior, facilitates retention of sexually motivated T-maze choice behavior in male rats, delays extinction of an appetitive discrimination task, affects approach behavior to an imprinting stimulus in ducklings, delays the postcastration decline in copulatory behavior in male rats, prevents or reverses amnesia induced by electroconvulsive shock, CO2 inhalation, pentylenetetrazol or puromycin. The majority of these effects may be explained by stimulatory influences of vasopressin on memory processes. Generally oxytocin exerts effects which are opposite to those of vasopressin and it has been suggested that oxytocin may be an amnesic neuropeptide. Evidence has been obtained that endogenous vasopressin and oxytocin play a physiological role in brain processes related to memory. Various limbic system structures seem to act as the anatomical substrate for the behavioral effects of vasopressin and different neurotransmitter systems seem to be involved. It is postulated that in case vasopressin affects retrieval processes the site of action is located in the amygdala and the dentate gyrus of the hippocampal complex with dopamine and serotonin as the respective neurotransmitter systems involved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypothalamic neuropeptides and memory. 399 53

Mucosal acidification (from pH 8.1 to 6.0) reversibly inhibited the hydroosmotic responses to oxytocin, cyclic AMP and 8-bromo-cyclic AMP in frog urinary bladder. These inhibitory effects were only observed in the presence of a permeant buffer in the apical medium and could also be elicited by CO2 bubbling, even when the mucosal pH was clamped at 8.1. Acid pH reduced the oxytocin-induced net water flux faster than norepinephrine or oxytocin removal and the difference was especially important at low temperature. The time course of recovery from acid pH inhibition was, at 20 degree C, similar to that of the hormonal action, but when the medium temperature was reduced to 6-7 degrees C, the recovery from acid pH inhibition paradoxically became faster while the oxytocin action was markedly slowed down (t 1/2 of changes in net water fluxes (expressed in min): oxytocin addition at 20 degrees C, 6.2 +/- 0.9; at 6 degrees C, 24 +/- 3; oxytocin removal at 20 degrees C, 4.7 +/- 0.8; at 6 degrees C, 22 +/- 3; pH inhibition at 20 degrees C, 2.6 +/- 0.2, at 6 degrees C 2.5 +/- 0.2; recovery from pH 6 at 20 degrees C 6.5 +/- 0.9; at 6 degrees C, 2.7 +/- 0.3). These results can be explained by accepting two main loci sensitive to medium acidification: (1) the cyclase system and (2) an intracellular, temperature-independent, post-cyclic AMP site. The fact that the intramembranous particle aggregates associated with the oxytocin-induced water permeability increase did not disappear after the flow inhibition by acid pH at low temperature suggests that the second effect could be located at the water channel itself.
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PMID:Cellular pH and water permeability control in frog urinary bladder. A possible action on the water pathway. 627 53

Urinary bladders of frogs were exposed to a transepithelial proton and osmotic gradient (serosal pH 8.1, Tris or bicarbonate buffer; mucosal pH 5.8, unbuffered) while the alkalinization rate of the mucosal bath and the net water movement were simultaneously monitored. It was observed that 1) the mucosal alkalinization rate was dependent on serosal pH and buffer; 2) oxytocin increased the mucosal alkalinization rate only when serosal bicarbonate was employed, whereas the net water movement augmented both when serosal bicarbonate or Tris buffers were used; 3) amiloride did not modify the mucosal alkalinization rate either before or after oxytocin; 4) the increases in the mucosal alkalinization rate and in the net water movement induced by oxytocin (serosal bicarbonate) were negatively correlated. In other experiments intracellular pH (pHi) was estimated with the DMO distribution technique with the following results. 1) Oxytocin increased the pHi when either serosal bicarbonate or Tris buffers was used and even in the presence of a low mucosal pH (Tris buffer, pH 5.8). 2) Important cellular acidification was observed when CO2 was bubbled (to pH 5.8), whereas the hydrosmotic response to 8-bromo-cAMP was clearly inhibited. These results indicate that cellular alkalinization could play a pivotal role in action of ADH, show that ADH can modify the transepithelial pH equilibrium mechanism, and suggest that intracellular pH regulation and water permeability control can be linked regulatory processes.
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PMID:Intracellular pH, transepithelial pH gradients, and ADH-induced water channels. 630 8

The hydrosmotic response elicited by oxytocin in the frog skin epithelium (Rana esculenta) was reversibly inhibited by 70% when the medium pH was reduced to 6.2 by CO2 bubbling on the serosal side. On the contrary, the response to 8-bromo cyclic AMP (8 Br-CAMP) was not affected by medium acidification, even after corion removal. In other experiments intracellular pH was measured, employing the dimetyl-oxazolidine-dione distribution technique, in frog urinary bladder and the isolated frog skin epithelium. As previously observed in the case of oxytocin, 8 Br-CAMP increased intracellular pH in frog urinary bladder. Incubation with oxytocin also augmented the intracellular pH in the isolated frog skin epithelium but 8 Br-CAMP did not modify cell proton concentration in this tissue. From previous and present results it can be summarized that: 1) The intracellular alkalinization effect elicited by oxytocin addition and the inhibition in the hydrosmotic response induced by medium acidification were qualitatively similar in both tested target epithelia. 2) On the contrary, a post cyclic AMP step sensitive to changes in intracellular pH was not observed in frog skin, as is the case in frog urinary bladder. 3) The 8 Br-CAMP induced intracellular alkalinization effect was only observed in frog urinary bladder.
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PMID:Cellular pH and the ADH-induced hydrosmotic response in different ADH target epithelia. 644 25

Uterine horns for castrated, estrogen-treated rats wee superfused for 6 hours in 95% O2/5% CO2 at 37 degrees C. The method of superfusion in which medium flows separately over the inner and outer surfaces of the horn allows prostaglandin synthesis in the myometrium and endometrium to be measured independently while their anatomical relationship is undisturbed. Prostaglandins were measured by radioimmunoassay. They myometrium formed more 6-keto-PGF1 alpha than PGF whereas the opposite was true of the endometrium. Production rates of TxB2 in both tissues were relatively low. The addition of inophore A-23187, oxytocin or phenylephrine to the superfusion medium not only increased the myometrial production rates of both 6-keto-PGF1 alpha and PGF but also increased the ratio of 6-keto-PGF1 alpha:PGF. Neither ionophore nor phenylephrine affected the rate of prostaglandin synthesis in the endometrium whereas oxytocin caused a significant increase in the production rate of PGF. We conclude that the large amounts of 6-keto-PGF1 alpha in the myometrial superfusate probably originate in both the smooth-muscle cells of the myometrium and the endothelium of the myometrial blood vessels. The differential responses to ionophore A-23187, phenylephrine and oxytocin suggest differences in the mode of their regulation of prostaglandin synthesis.
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PMID:Differential production of PGF and 6-keto-PGF1 alpha by the rat endometrium and myometrium in response to oxytocin, catecholamines and calcium ionophore. 677 83

The effect of angiotensin II and [Sar1,Ile5,Ala8]-angiotensin II on uterine contractions and the relationship of uterine prostaglandins to these effects were studied. Uterine segments from pregnant rats were monitored in vitro for isometric contractile activity in Krebs-Ringer medium (95% O2-5% CO2; 37 C). The medium was sampled periodically and assayed for prostaglandin E2, prostaglandin F2 alpha, and 13,14-dihydro-15-keto-prostaglandin F2 alpha by RIA. Angiotensin II increased frequency of contractions and integrated contractile force in a dose-related fashion. Angiotensin II (1 microgram) resulted in increased prostaglandin (PG) production, but there was no clear dose-related effect. Indomethacin significantly reduced PG production (P < 0.001); however, the contractile response to angiotensin II was not affected. [Sar1,Ile5,Ala8]Angiotensin II had no effect on spontaneous contractile activity or PG production in uteri from 18 or 21 days of pregnancy, nor did [Sar1,Ile5,Ala8]angiotensin II affect oxytocin-stimulated uterine contractions. [Sar1,Ile5,Ala8]Angiotensin II (2.5 microgram) did inhibit (P < 0.05) uterine contractions induced by angiotensin II (0.5 microgram), but PG production was not affected. In conclusion, the studies described provide evidence that angiotensin II-induced uterine contractions of in vitro pregnant rat uteri are not dependent upon increased PG production.
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PMID:Angiotensin II and [Sar1, Ile5, Ala8]angiotensin II effect on contractile activity and prostaglandin production of in vitro pregnant rat uteri. 742 93

This experiment was designed to study the effects of cell-to-cell contact, arachidonic acid (10 microM; AA), oxytocin (10 microM), and luteinizing hormone (5 ng; LH) on bovine luteal cell function. Corpora lutea collected from Holstein cows between Days 10 and 12 (n = 4; midluteal stage) or 17 and 18 (n = 4; late-luteal stage) of the estrous cycle (Day 0 = estrus) were dispersed, and small and large cells were separated by unit gravity sedimentation and flow cytometry. Large and small luteal cells were either incubated together, allowing intercellular contact, or separately, without intercellular contact, with culture well inserts. Cells were incubated in a modified Ham's F-12-N-hydroxyethylpiperazine-N'-2-ethanesulfonic acid medium. After an 18-hr preincubation period, treatments were introduced and cells were incubated for 240 hr. Media samples were collected and treatments were replaced at 48-hr intervals. Incubations were maintained at 37 degrees C in 5% CO2 in humidified air. Overall, progesterone secretion decreased with increased incubation time (P < 0.0001), regardless of treatment, stage of the cycle, or cell arrangement. During the 18-hr pretreatment period, large and small luteal cells with contact secreted more progesterone than did luteal cells without contact during both the mid- (P < 0.0001) and late-luteal stages (P < 0.06) of the estrous cycle. After treatments were initiated, both mid- and late-stage luteal cells treated with LH secreted more (P < 0.0001) progesterone than occurred with any other treatment; oxytocin, AA, and control treatments were similar.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contact-associated interactions between large and small bovine luteal cells during the estrous cycle. 762 77

Antidiuretic hormone and parathyroid hormone (PTH) inhibit HCO3- absorption by the rat medullary thick ascending limb (MTAL). Studies were performed on rat MTAL tubule suspension to specify the H(+)-HCO3- membrane transporters affected by these hormones and the implicated intracellular second messengers. Arginine vasopressin (AVP) and PTH stimulated cell adenosine 3',5'-cyclic monophosphate (cAMP) production with a relative rank order potency of AVP > rat PTH-(1-34) > bovine PTH-(1-84). Significant cell acidification in HCO3- -CO2-free medium, monitored in 2'7'-bis(carboxyethyl)-5(6')-carboxyfluorescein-loaded cells, was caused by 0.1 nM AVP, 1 nM rat PTH-(1-34), but not by < 100 nM bovine PTH-(1-84), as well as by 10(-4) M 8-bromo-cAMP and 2 x 10(-5) M forskolin; 10 nM AVP or rat PTH-(1-34) did not alter the intracellular pH when Na+/H+ antiport was inhibited by 2 mM amiloride. Prostaglandin E2 (PGE2, 10(-6) M), which inhibited AVP-stimulated cell cAMP production, reduced by 35% the cell acidification response to 10 nM AVP. AVP and 8-bromo-cAMP inhibited Na+/H+ antiport-dependent cell pH recovery from intracellular acidification, which was explained by a decrease in the Vmax of the antiporter. AVP did not directly affect K(+)-HCO3- cotransport and plasma membrane H(+)-ATPase of rat MTAL cells. Cytosolic calcium ([Ca2+]i), monitored in fura-2-loaded cells, was unaffected by up to 1 nM AVP, 100 nM PTH, glucagon, calcitonin, and oxytocin, and 1 microM PGE2; however, 100 nM AVP, but not 1-desamino-8-D-AVP (dDAVP), caused a peak increase in [Ca2+]i, even in the absence of extracellular Ca2+, and stimulated cell accumulation of [3H]inositol phosphates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:cAMP-dependent control of Na+/H+ antiport by AVP, PTH, and PGE2 in rat medullary thick ascending limb cells. 838 52

This study aimed to investigate if pregnancy-induced hypoalgesia occurs in the sow, and to examine the role of endogenous opioids which are known to be released in response to nociception. Sixteen Large White x Landrace multiparous sows were tested in straw bedded pens (2.5 x 2.5 m) during weeks 4, 8 and 12 of pregnancy and over the farrowing period. Testing involved thermal stimulation of eight areas on the rear-quarters of the sows with a CO2 infra-red laser until a physical response was seen (tail flick, leg move or muscle twitch) or for a maximum of 16 s. Over the farrowing period testing was more frequent, and at 3.75 h after the birth of the first piglet, half the sows received an injection (i.m.) of an opioid antagonist naloxone (N) (1 mg kg(-1) body weight) with the remainder receiving a control dose of saline (S). Responses were recorded 15 and 30 min post-injection. There was no significant difference between response times over weeks 4, 8 and 12 of pregnancy (P = 0.152), however a significant rise was seen from week 12 to 5 days before parturition (P = 0.002). Response times continued to rise until the birth of the first piglet by which time the majority of sows had stopped responding within 16 s (P < 0.001). Response times fell over days 1, 2 and 7 post-partum. After administration of naloxone response times fell compared to control animals at 15 min (P < 0.001) and 30 min (P < 0.01) post-injection. These results suggest that nociceptive threshold increases during late pregnancy in the sow, perhaps as an endogenous defence against labour pain, and that during parturition this change in nociceptive threshold is, at least in part, opioid-mediated. Oxytocin is known to be inhibited by endogenous opioids at parturition, thus future research should consider the potential role of increased nociception at birth as a negative feedback to oxytocin release.
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PMID:Opioid-mediated changes in nociceptive threshold during pregnancy and parturition in the sow. 927 99


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