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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A low concentration (0.2 nM) of oxytocin induced phasic tension development in the isolated uterus of the day-22 pregnant rat. Tonic spasm was also induced by higher concentrations of oxytocin (2 and 20 nM). Spasmogenic responses to bradykinin and potassium chloride (KCl) also contained phasic and tonic components while acetylcholine induced tonic spasm only. The phasic component of the responses to oxytocin and to bradykinin and both components of the response to KCl were inhibited by (+)-cis diltiazem (0.1 and 1 microM). The tonic component of the responses to oxytocin and to bradykinin and the responses to acetylcholine were only reduced by (+)-cis diltiazem at concentrations greater than 10 microM. (-)-cis Diltiazem was less potent than (+)-cis diltiazem as an inhibitor of calcium (Ca2+)-induced spasm in a depolarizing medium and of the phasic spasms induced by oxytocin. The two isomers were of similar potency as inhibitors of oxytocin-induced tonic spasm. Spasmogenic responses to oxytocin, bradykinin, acetylcholine and KCl were decreased when uteri were bathed in media which were Ca2+-free or of low Na+ content. However, there was no correlation between the rank order of sensitivity of the four spasmogens to the changed media and to their inhibition by (+)-cis diltiazem. Oxytocin (0.2 nM) increased the frequency, duration and amplitude of spike activity, measured by extracellular electrical recording, in parallel with enhancement of phasic tension development. With higher concentrations of oxytocin (2 and 20 nM) spike firing was initially continuous but often subsequently ceased despite the associated tonic contracture. After incubation in (+)-cis diltiazem (10 microM), oxytocin (0.2, 2 and 20 nM) produced graded tonic spasm without spike activity. Oxytocin (0.2 nM) produced a small increase in 45Ca2+ influx into myometrium as assessed by the 'lanthanum method'. Higher concentrations of oxytocin (2 and 20 nM) did not increase 45Ca2+ influx. It is concluded that the phasic component of the response of the uterus to oxytocin and bradykinin is associated with Ca2+ influx via voltage-dependent Ca2+ channels. The tonic component is due to another mechanism(s) which does not appear to involve Ca2+ influx. All of the spasmogenic response to KCl can be explained by Ca2+ influx through voltage-dependent Ca2+ channels. These channels do not appear to be involved in the spasmogenic response to acetylcholine.
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PMID:The spasmogenic action of oxytocin in the rat uterus--comparison with other agonists. 374 62

Spontaneous intracellular electrical activity and contraction of pregnant human myometrium were recorded by the single sucrose-gap method, and the effects of oxytocin on the muscle were studied. In pregnant human myometrium at term, both plateau and spike types of action potentials were observed. All contractions were well synchronized with each action potential. Oxytocin, 10(-2) U/ml, potentiated spontaneous contractions by enhancing the plateau part of action potentials; spike-type configuration became plateau. When extracellular ionized calcium was removed, spontaneous activities disappeared, while 10(-2) U/ml of oxytocin could evoke action potentials and contractions but these were smaller than those of the controls. Spontaneous activities also disappeared when ionized calcium was increased to 5 mmol/L, but oxytocin evoked plateau potentials and contractions remarkably. Diltiazem (ionized calcium antagonist), 10(-6) gm/ml, suppressed the spontaneous activity, but oxytocin evoked action potentials and contractions in high frequency, the duration of the action potential being short and the contraction being small. In the presence of 10(-4) gm/ml of diltiazem, 10(-2) U/ml of oxytocin could not evoke any action potentials but did evoke small and long contractures, while in a high ionized potassium contracture experiment, oxytocin potentiated the tonic phase. These results suggest that oxytocin can increase spontaneous contractions by enhancing plateau potentials and that this effect requires sufficient extracellular ionized calcium. In this potentiation, the effects on frequency and amplitude of contractions might vary. It is also suggested that oxytocin may evoke a contracture in the absence of an action potential by releasing calcium from intracellular storage sites.
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PMID:Effect of oxytocin on spontaneous electrical and mechanical activities in pregnant human myometrium. 375 87

To determine the effects of fluid restriction in induced labour with oxytocin in 5% dextrose solution, maternal venous blood and fetal cord venous blood were examined in 164 mothers in induced labour and 29 mothers with a spontaneous onset of labour. After satisfactory uterine activity was induced either the oxytocin infusion was managed according to routine delivery unit practice (n = 36), or infusion rates were halved (n = 45), or quartered (n = 43), or discontinued (n = 40). Despite fluid restriction during labour the mean sodium concentration in maternal blood or cord blood had fallen to a similar extent in all four induced groups at delivery. Potassium, urea, creatinine, total protein, and albumin in maternal blood or cord blood were affected differently by induced labour as compared with sodium. The fall in sodium concentration in maternal blood was a more consistent reflection of the total volume of fluid received, mean infusion rates and cord blood sodium after infusion rates were quartered or discontinued. The incidence of hyponatraemia was 5% in mothers and 8% in infants. A comparison of hyponatraemic and normonatraemic cord blood showed no significant differences in serum bilirubin levels or red cell counts, but more hyponatraemic infants developed neonatal jaundice. It is suggested that in induced labour fluid restriction alone does not prevent hyponatraemia and neonatal jaundice.
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PMID:Oxytocin induction of labour: hyponatraemia and neonatal jaundice. 377 Feb 80

Synthetic oxytocin (OT) was infused iv in four men at 3 mU/min, and the rate was doubled every 90 min for a total of three infusion periods. The mean (+/- SEM) OT MCR was 16.4 +/- 1.7 ml/kg X min and was independent of the rate of infusion. A method for measuring OT in urine was developed using an octadecasilyl-silica column for extraction of the hormone. The extracted residue was reconstituted in potassium phosphate buffer, pH 7.4, for RIA. The minimum detectable level of OT in urine was 0.2 microU/ml (defined as a bound to free ratio of approximately 90%). The mean recovery of OT was 77 +/- 2%. The mean (+/- SEM) concentration of endogenous OT in urine was 10.2 +/- 1.4 microU/ml. Endogenous OT in urine eluted from a reverse phase high pressure liquid chromatography column as a single peak of OT immunoreactivity in the position of synthetic OT. Urinary OT excretion during infusion of synthetic OT was linearly correlated with plasma OT concentration whether calculated as microunits of urinary OT per mg creatinine (r = 0.89) or urinary OT per min (r = 0.93). Mean urinary fractional clearance of OT (OT clearance/creatinine clearance) was 3.6% renal clearance of OT (5.5 ml/min or 0.43% of MCR). Thus, OT MCR was constant over a wide range of physiological plasma OT levels and was similar to MCR in pregnant women studied previously in this laboratory. Less than 1% of OT was cleared in urine. This study defines the relationship between urinary and plasma OT during steady state infusion of physiological concentrations of the hormone and indicates that measurements of OT in urine by RIA may prove helpful for pharmacokinetic and physiological studies of OT-related events in humans.
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PMID:Clearance studies of oxytocin in humans using radioimmunoassay measurements of the hormone in plasma and urine. 379 53

Changes in the mineral composition of mare milk during lactation were studied. Milk samples were obtained from five Thoroughbred mares one to three times weekly from the first to the eighth week of lactation and from two of the mares for an additional 8 wk. Samples averaging 500 mL were obtained after oxytocin was administered to the mares. Each sample was analyzed for total solids, ash, calcium, phosphorus, magnesium, sodium, potassium, copper and zinc. The concentration of all constituents except sodium and potassium decreased throughout lactation. The rates of decline of ash, calcium, phosphorus and magnesium concentration were similar, but the rates of decline of the other elements differed. Thus, the mineral composition of mare milk should be described in terms of the stage of lactation of the mare. The total solids and ash content of mare milk were 12 and 0.61% respectively, at the end of the first week of lactation, 10.5 and 0.45% at 4 wk, 10 and 0.38% at 8 wk and 10.2 and 0.32% at 16 wk. The calcium, phosphorus and magnesium concentrations at the end of the same periods were 1345, 943 and 118 micrograms/g of milk at 1 wk; 1070, 659 and 86 at 4 wk; 831, 574 and 58 at 8 wk and 700, 540 and 43 micrograms/g of milk at 16 wk. Copper and zinc concentrations were 0.85 and 3.1, 0.55 and 2.2, 0.29 and 1.9 and 0.28 and 1.8 microgram/g of milk at 1, 4, 8 and 16 wk, respectively.
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PMID:Lactation in the horse: the mineral composition of mare milk. 379 22

An assessment was made of the potencies of nifedipine, gallopamil, diltiazem, cinnarizine and salbutamol as inhibitors of tension development by the uterus and cardiovascular tissues from the term pregnant rat. The rank order of potency was nifedipine greater than gallopamil greater than diltiazem for those preparations on which these compounds were potent, viz. spontaneous and oxytocin-induced tension development of the uterus, spontaneous tension development of hepatic portal vein, potassium chloride (KCl)-induced pressure rises of perfused mesenteric bed and electrically-stimulated (0.5 Hz) ventricular muscle. The rank order of potency of nifedipine, gallopamil and diltiazem was different for those preparations on which they exhibited low potency, viz. noradrenaline-induced pressure rises of perfused mesenteric bed and tension development of aorta. Gallopamil and diltiazem, but not nifedipine, were more potent against tension development by ventricular muscle stimulated at 2.5 Hz than at 0.5 Hz, suggesting that nifedipine interacts at a different site from the other compounds. Cinnarizine was less potent than the other calcium antagonists on the uterus and portal vein, was the second most potent compound against KCl-induced pressure rises of the mesenteric bed and was equipotent against responses to noradrenaline and KCl of the mesenteric bed (unlike the other compounds). This suggests that the site of action of cinnarizine differs from that of the other calcium antagonists. Nifedipine, gallopamil and diltiazem, like salbutamol, exhibited selectivity for inhibition of tension development by the uterus relative to the cardiovascular tissues.
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PMID:A comparison of several calcium antagonists on uterine, vascular and cardiac muscles from the rat. 402 68

1. Strips of longitudinal muscle can be obtained from guinea-pig ileum either retaining or free from Auerbach's plexus.2. The denervated strip is unresponsive to electrical stimulation by brief shocks, whether given singly or in trains; it also fails to respond to nicotine or dimethylphenylpiperazinium iodide (DMPP), and eserine causes no spasm.3. Denervated strips neither contain detectable acetylcholine (< 0.4 ng/mg), nor release it spontaneously (< 5 pg/mg/min) or in response to stimulation (< 31 pg/mg/min). The acetylcholine metabolism of the innervated strip is therefore that of the adherent Auerbach's plexus. Innervated strips had a mean acetylcholine content of 28 ng/mg, a mean resting output of 94 pg/mg/min and an output in response to stimulation at 10 c/s of 700-1200 pg/mg/min.4. By comparing the responses of innervated and denervated strips it was concluded that arecoline, methylfurmethide, alpha,beta-ethylal-gamma-tri-methylammonium propanediol iodide (2268 F), muscarine, histamine, tremorine, oxytocin, and substance P, like acetylcholine, act primarily on the smooth muscle directly; and that angiotensin, barium, potassium, m-bromophenyl choline ether and 5-hydroxytryptamine have a progressively increasing proportionate effect on the nerve plexus. Nicotine and DMPP were inactive in the absence of the plexus.5. The longitudinal muscle with its accompanying plexus contains about one quarter of the acetylcholine of the whole ileum, and is responsible for about one fifth of the output to electrical stimulation.6. The volley output of acetylcholine by the innervated strip declines sharply as rate of stimulation increases. Output of acetylcholine was reduced by morphine and by cocaine, particularly when resting or when stimulated at low rates.7. Acetylcholine output by whole ileum from guinea-pig declines in the absence of glucose, but is insulin-independent. Output by strips of ileum from rats made diabetic with alloxan was similar to that from normal rats.8. The similarity in properties of acetylcholine output from innervated strips, where it must come from nervous tissue, to that from whole ileum, and the insulin-independence of output from whole ileum suggest that the whole of the acetylcholine output of intestine is nervous in origin.9. Comparison of the acetylcholine metabolism of the innervated strip with that of the superior cervical ganglion suggests that the typical features of the former (high resting output, high volley output at low rates, low minute output at high rates of stimulation, and sensitivity to morphine) may be linked with the absence of specialized neuro-effector junctions and represent a relatively primitive transmission process.
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PMID:The origin of acetylcholine released from guinea-pig intestine and longitudinal muscle strips. 429 53

A newly devised dual labeled iodine isotopic method is described for the detection and quantitation of alterations in thyroxine (T(4)) deiodination rate in man. This method employs the principle of a constant (125)I infusion to serve as a reference source for the generation of (131)I derived from the deiodination of T(4)-(131)I. Measurement of these two iodide isotopes are made in serially timed urine collections and are expressed in terms of a ratio value. Using this technique, it was possible to measure accurately the effects of a single dose of 6-propylthiouracil (6-PTU) in producing inhibition of T(4) deiodination in euthyroid subjects. It was also possible to assess the time of onset, duration of action, and degree of inhibition produced by 6-PTU. Employing single doses of 6-PTU, ranging from 100 to 1000 mg, there was found to be a log dose relationship with a degree of inhibition observed in T(4) deiodination. In control studies T(4) deiodination rate was found to be constant for periods ranging up to 72 hr in normal ambulating subjects. The acute administration of many other agents was employed in an attempt to alter the T(4) deiodination rate. These included diphenylhydantoin, methimazole, triiodothyronine, thyroxine, thyroid stimulating hormone (TSH), adrenocorticotropin (ACTH), hydrocortisone, predinsolone, potassium iodide, epinephrine, and oxytocin. No detectable change in T(4) deiodination rate was observed with these agents in the dosage ranges employed in this study. The lack of any observable alteration in the T(4) deiodination rate in response to this array of drugs and hormones appears to indicate that the availability of T(4) to intracellular sites of deiodination and possibly action is well modulated to resist abrupt changes.
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PMID:A new method for the measurement of acute alterations in thyroxine deiodination rate in man. 431 46

1. The effect of intravenous infusions of various ions on the antidiuretic action of antidiuretic hormone has been studied in rats.2. Lithium (13 mmol/l.) reversibly inhibits the antidiuretic responses. Similar concentrations of potassium, rubidium, strontium, magnesium, choline and calcium do not. Lithium has a similar effect on the antidiuretic activity of oxytocin.3. The inhibition is not simply related to blood nor whole body lithium concentrations.4. Lithium (2 mmol/l.) in contact with the serosal surface also inhibits the transport of water facilitated by either 0.5 U/l. antidiuretic hormone or 1.1 mmol/l. cyclic adenosine monophosphate in the isolated toad bladder.5. Choline (2 mmol/l.) on the serosal surface also inhibits the transport of water facilitated by vasopressin in the toad bladder.
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PMID:Some aspects of the inhibition of the action of antidiuretic hormone by lithium ions in the rat kidney and bladder of the toad Bufo marinus. 435 11

1. Contractions of guinea-pig isolated proximal colon produced by vasopressin are not affected by methyloxytocin (a compound that blocks pressor effects of vasopressin).2. Vasopressin contractions are inhibited by replacement of sodium with mannitol or sucrose, elevation of potassium or magnesium concentrations, the presence of the metabolic inhibitors sodium azide and triethyl tin or tetrodotoxin in the bathing fluid. Contractions produced by histamine or choline esters are comparatively insensitive to these procedures.3. Contractions of rat isolated uterus following vasopressin, oxytocin and methacholine are equally affected by replacement of sodium, increase of potassium or magnesium or addition of sodium azide.4. Neither vasopressin contractions nor contractions caused by transmural stimulation were consistently affected by morphine (10(-6) g/ml.) or hyoscine (10(-7) g/ml.) although both were reduced by anoxia or cooling the tissue. Morphine did not reduce the output of acetylcholine from stimulated colon.5. It is concluded that the action of vasopressin on proximal colon is unlike its action on other smooth muscle and is mediated by nervous tissue.
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PMID:Studies on the mode of action of vasopressin on the isolated proximal colon of the guinea-pig. 534 54


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