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

Bovine granulosa cells were treated in culture with alpha- and beta-adrenoceptor ligands to determine the receptor subtype mediating their response to catecholamines. The secretion of oxytocin by granulosa cells in serum-free medium was measured on the fourth day of culture (during the period of acquisition of a luteal phenotype). Cultures were performed in the presence of 0.5 mM ascorbic acid, which increased hormone output and potentiated the response to catecholamines. The effects of adrenaline and noradrenaline on oxytocin secretion were concentration-dependent; maximum stimulation was over 700% with adrenalin (EC50 92 nM) and 500% with noradrenaline (EC50 87 nM). The response to noradrenaline (10(-6) M) and adrenaline (10(-6) M) could be blocked by propranolol but not by phentolamine, suggesting that beta- rather than alpha-adrenoceptors were involved. Blockade by metoprolol and practolol (beta 1-adrenoceptor antagonists) was poor and dobutamine (beta 1-agonist) was weakly stimulatory. A concentration-dependent stimulatory response (EC50 200 nM) was obtained with salbutamol (beta 2-adrenoceptor agonist) and stimulation by adrenaline or salbutamol could be blocked by a selective beta 2-adrenoceptor antagonist (ICI 118,551). It is concluded that, during luteinization, the long-term response of bovine granulosa cells to stimulation induced by catecholamines is mediated through beta- rather than alpha-adrenoceptors. Although the beta 2-subtype is probably involved, the similar potencies of adrenaline and noradrenaline are uncharacteristic of beta 2-adrenoceptors and may be peculiar to the long-term response shown by these cells.
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PMID:Beta adrenoceptors mediate the catecholamine-induced stimulation of oxytocin secretion from cultured bovine granulosa cells. 168 97

1. Intracellular current and voltage clamp recordings were obtained from rat supraoptic nucleus neurones in superfused hypothalamic explants in order to evaluate their response to dopamine and to D1 and D2 agonists. 2. With one exception, exposure to dopamine (10-200 microM) depolarized supraoptic neurones. When tested for an effect on twenty-one spontaneously active supraoptic neurones, dopamine enhanced the firing of all eleven continuous-firing (possibly oxytocin-secreting) neurones and prolonged the burst in all ten phasic-firing (vasopressin-secreting) neurones. 3. In sixty-seven of sixty-eight neurones where current injection was used to maintain membrane potential below threshold for action potential generation, current clamp data revealed that exposure to dopamine (10-200 microM) was followed in 10-17 s by a gradual 3-7 mV membrane depolarization that lasted for 4-15 min and was accompanied by a 12-23% reduction in input resistance. Exposure to quinpirole, a D2 agonist (10-200 microM), induced a similar response with comparable onset, duration and change in input resistance. In contrast, tests on sixteen cells indicated little or no response to a D1 agonist SKF38393. 4. Under voltage clamp, dopamine was noted to induce an inward current, accompanied by a 7.5-40% increase in membrane conductance over the corresponding time course. 5. Voltage-current plots for dopamine-induced depolarizations were linear in the range -50 to -110 mV. Dopamine and quinpirole depolarizations had extrapolated mean reversal potentials of -25 +/- 10 mV (mean +/- S.D.) and -20 +/- 15 mV respectively. This approximated the mean reversal potential of -20 +/- 8 mV measured from the dopamine-induced inward current using single-electrode voltage clamp. 6. The actions of dopamine were selectively antagonized by two D2 receptor antagonists, sulpiride and spiperone, but neither influenced membrane depolarizations induced by equimolar concentrations of noradrenaline. Dopamine-induced depolarizations also persisted following selective blockade of alpha 1-adrenergic receptors by prazosin; under these conditions, noradrenaline induced membrane hyperpolarization. 7. Following complete substitution of external Na+ with Tris, the reversal potential for the dopamine-induced response was shifted to -70 +/- 9.8 mV. This value was consistently less negative than the estimated potassium equilibrium potential. 8. The depolarization action of dopamine persisted in media containing tetrodotoxin and with an external calcium concentration ([Ca2+]o) of 0 mM-Ca2+ with 6 mM-Mg2+ or Mn2+, but was abolished following intracellular injection of [1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), a Ca2+ chelator.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Dopamine D2 receptor activation depolarizes rat supraoptic neurones in hypothalamic explants. 168 25

We investigated the effects of synthetic human relaxin (hRLX-2) on isolated rat and human myometrium and on uteroplacental arteries from term pregnant women. The preparations were mounted in organ baths and isometric tension was recorded. In isolated myometrium from nonpregnant rats, hRLX-2 (10(-10)-10(-7) mol/L) produced concentration-dependent inhibition of contractile activity induced by vasopressin (10(-8) mol/L). In isolated human myometrium from the fundus or isthmus, hRLX-2 (10(-10)-10(-7) mol/L) did not influence spontaneous activity or contractions induced by oxytocin (10(-9) mol/L) and prostaglandin (PG) F2 alpha (10(-5) mol/L). Nor did it influence the tension induced in small intramyometrial arteries by U46619 (10(-7) mol/L), noradrenaline (10(-5) mol/L), and endothelin (10(-9) mol/L); or the tension induced in fetal stem villus arteries by U46619 (10(-7) mol/L), endothelin (10(-9) mol/L), and PGF2 alpha (10(-5) mol/L). The inhibitory effects of hRLX-2 in preparations of rat myometrium were not influenced by the presence of human myometrium in the organ bath or by pre-incubation of hRLX-2 with human myometrium. These results suggest that direct inhibitory effects of relaxin may be of minor importance for the regulation of myometrial activity and uteroplacental circulation in term human pregnancy.
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PMID:Effects of human relaxin on isolated rat and human myometrium and uteroplacental arteries. 192 92

1. The effect of tetrodotoxin (5 microM), monensin (10 microM) and the replacement of Na+ by choline (choline medium) on the contractions of the rat testicular capsule induced by oxytocin (50 and 200 nM) have been studied. 2. The sodium channel blocker tetrodotoxin did not modify the oxytocin contraction. 3. The sodium ionophore monensin produces contraction of rat testicular capsule and reduces the oxytocin-induced contraction. The monensin contraction is inhibited by amiloride (0.1 mM). 4. Replacement of Na+ by choline increases the contraction induced by oxytocin and KCl (60 mM) but inhibits that induced by noradrenaline (3 microM). 5. The increase of contraction due to oxytocin in choline medium is inhibited by amiloride (50 microM and 1 mM) and when calcium is suppressed of the incubation medium.
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PMID:Influences of sodium on the contraction induced by oxytocin in rat testicular capsule. 193 6

Central neurotransmitter and/or neuromodulator candidates reported to affect gastric acid secretion are: (excitatory) acetylcholine, thyrotropin releasing hormone, GABA, oxytocin; (inhibitory) noradrenaline, adenosine, bombesin, calcitonin-gene related peptide, corticotropin releasing factor, beta-endorphin, neurotensin, neuropeptide Y, insulin-like growth factor II and prostaglandins. Regulation of gastric acid secretion by central administration of these substances in experimental animals such as rats and dogs are briefly reviewed, and central inhibitory mechanisms of this function are discussed based on our studies with noradrenaline and bombesin. Roles of hypothalamic nuclei such as the ventromedial nucleus and the lateral hypothalamus in regulation of autonomic nerve activities are also described as an introductory note.
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PMID:[Central neurotransmitters and regulation of gastric acid secretion]. 198 Jun 59

The intrinsic innervation of the human uterine artery was investigated histochemically, and the motor responses to some of the demonstrated peptides and other humoral factors were studied on isolated vascular preparations. There were nerves with specific immunoreactivities for tyrosine hydroxylase, dopamine beta-hydroxylase, neuropeptide-Y (NPY), vasoactive intestinal peptide (VIP) and peptide histidine methionine, and enzymatic reactivity for acetylcholine esterase. The most effective stimulator of smooth muscle contractility was arginine vasopressin followed in order by oxytocin, noradrenaline together with NPY, noradrenaline alone and dopamine. No effect was seen with acetylcholine and tyrosine, and VIP caused inconsistent relaxation of contractile activity induced by PGF2 alpha. These results suggest that the uterine blood flow is regulated by complex interactions of factors, some occurring in nerve terminals and some being circulating humoral factors.
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PMID:Innervation of the human uterine artery and contractile responses to neuropeptides. 201 Jan 12

Uterine contractions in labour are influenced by endogenous substances such as oestrogens, progesterone, cortisol, oxytocin, prostaglandins, relaxin, adrenergic and cholinergic secretions, cyclic nucleotides and calcium ions. Effects of progesterone and oestrogens are complimentary as well as antagonistic to each other. They regulate formation of gap junctions, influx of calcium ions, synthesis of oxytocin, adrenergic receptors and of prostaglandins and cyclic nucleotides. Cortisol shares a role in a more complex endocrine trigger but is ineffective alone in the initiation of human labour. Adrenaline inhibits and noradrenaline promotes uterine contractions. Cholinergic stimulation increases cyclic GMP promoting uterine contractions. Calcium ions play a key role in uterine contractility. Oxytocin, prostaglandins E and F are powerful stimulants of uterine contractions. Prostaglandins stimulate pregnant uterus from early gestation unlike oxytocin which has little effect in the first and second trimester. They are extensively used for initiating labour and to arrest intractable atonic postpartum haemorrhage. In experiments and in vivo, their effects are modulated by other hormones and substances. With discovery of new drugs, knowledge of how they act on the uterus becomes important. The pharmacology of parturition that may help to understand the interaction of various agents on the pregnant uterus has been discussed.
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PMID:Pharmacology of parturition. 202 68

Bovine corpora lutea and ovarian stroma were analysed by high-performance liquid chromatography for catecholamine content. High concentrations (up to 102 nmol/g wet weight) were found in both 'central' stroma, containing many blood vessels, and 'peripheral' stroma. Central stroma contained noradrenaline and some dopamine, whereas peripheral stroma contained a higher proportion of dopamine and also significant amounts of 3,4-dihydroxyphenylacetic acid (DOPAC). Occasional samples of stroma had very high amounts of dopamine, suggesting that it is stored in specific regions. Corpora lutea, although devoid of direct innervation, contained dopamine (up to 5.3 nmol/g) and noradrenaline (up to 1.2 nmol/g). The average dopamine:noradrenaline molar ratio was 1.19:1 and the concentrations of dopamine and noradrenaline were highly correlated (P less than 0.002). The concentration of dopamine was significantly higher in the early luteal phase of the oestrous cycle than during the rest of the cycle or in pregnancy. The levels of noradrenaline and dopamine present in corpora lutea are sufficient to modulate the production of both oxytocin and progesterone by luteal cells in vitro.
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PMID:Regional differences in catecholamine concentrations in bovine ovaries analysed by high-performance liquid chromatography. 204 Aug 56

Antibodies to oxytocin and noradrenalin were utilized in an immunocytochemical study of the caudal ventrolateral medulla of the rat brainstem. Noradrenalin was visualized by using antibodies to noradrenalin and by means of a silver-gold intensification of diaminobenzidine, whereas oxytocin could be demonstrated in the same section by using the diaminobenzidine precipitate as a marker. At the light microscopic level, oxytocin fibers were densely distributed around the A1 cell bodies. At the ultrastructural level, oxytocin-containing fibers were seen to terminate synaptically onto noradrenalin-containing neurons. Previous studies have shown that electrical stimulation of A1 neurons selectively activates vasopressin-secreting neurons in the supraoptic nucleus. Therefore, separate electrophysiological studies were set up, in which we observed that oxytocin infusions (100-200 pg) into the A1 area enhanced the activity of 16 out of 19 putative vasopressin-secreting neurons and elicited no response from any of 10 oxytocin-secreting neurons. This finding suggests that some of the parvicellular neurons in the paraventricular nucleus of the hypothalamus, from which the A1 neurons derive their oxytocin innervation, can activate the A1 cell group via this peptidergic neurotransmitter. One of the consequences of A1 neuronal activation is enhanced firing of hypothalamic supraoptic (and paraventricular) vasopressin-secreting neurons, and a consequent rise in plasma vasopressin.
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PMID:Oxytocin localization and function in the A1 noradrenergic cell group: ultrastructural and electrophysiological studies. 209 24

Release of oxytocin by sliced or minced sheep luteal tissue in vitro was stimulated up to 1.6- and 2.3-fold by arachidonic acid and the calcium ionophore A23187 respectively. Prostaglandin (PG) F2 alpha and the PGF2 alpha analogue cloprostenol, and other potential agonists known to be active in vivo, including noradrenaline and acetylcholine, were ineffective, as was the phorbol ester tetradecanoylphorbol acetate (TPA). The ineffectiveness of PGF2 alpha was not due to a general unresponsiveness of the tissue in vitro, as PGF2 alpha reduced LH stimulation of tissue concentrations of cyclic AMP and activated inositol lipid hydrolysis. The effect of arachidonic acid was accompanied by release from the tissue of the cytosolic enzyme lactate dehydrogenase (at arachidonic acid concentrations below those required to release oxytocin) and its effect on oxytocin and lactate dehydrogenase release was mimicked by oleic and linolenic acids; arachidonic acid was concluded to act by a non-physiological physicochemical effect without conversion to an eicosanoid. As PGF2 alpha in vitro is known to raise intracellular Ca2+ concentrations in the large luteal cells that secrete oxytocin, and as A23187 stimulates oxytocin release in vitro in the presence and absence of TPA, it is concluded that in-vitro incubation results in an artifactual blockade of the oxytocin-releasing action of PGF2 alpha at an unidentified point distal to the effect on intracellular Ca2+.
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PMID:Effects of prostaglandin F2 alpha and other potential secretagogues on oxytocin secretion and second messenger metabolism in the ovine corpus luteum in vitro. 216 27


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