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

1. We have investigated changes in extracellular potassium concentration [K+]o in the supraoptic nucleus of lactating rats and in particular those that occur during the intense burst of firing by the oxytocin neurones involved in the milk ejection reflex. 2. Double-barrelled K(+)-selective microelectrodes containing a highly selective sensor based on valinomycin were lowered through the exposed cortex towards the supraoptic nucleus (SON) of female rats anaesthetized with urethane. The mean resting [K+]o in the hypothalami of five rats was 2.4 mM, S.D. = 0.3 mM. 3. Where the reference barrel recorded extracellular action potentials from an oxytocin cell, the reflex burst of firing (4 s, typical maximum 50 Hz) was accompanied by a mean increase in [K+]o (delta[K+]o) of 0.22 mM (S.E.M. = 0.02 mM, fifty-seven bursts in eight cells in seven rats). The rise in [K+]o did not begin more than 0.1 s before the onset of the burst, and began to fall from its maximum during the burst. Slow field potentials, indicative of spatial buffering of K+, were undetectable (less than 50 microV). When the electrode was advanced in steps, the amplitudes of both delta[K+]o and the action potential declined steeply to about 10% over a distance of 20 microns: K+ from oxytocin cells appears to be prevented from dispersing freely through the extracellular space of the SON. 4. When the electrode recorded action potentials from a vasopressin cell, delta[K+]o during an oxytocin cell burst was very small: 0.021 mM (S.E.M. = 0.005 mM). At other sites in the SON, where antidromic stimulation evoked a field potential but no action potential, delta[K+]o was 0.047 +/- 0.005 mM. We conclude that the reason oxytocin bursts do not affect vasopressin cells is that [K+]o rises very little around vasopressin cells. A fortiori, since the increases in [K+]o were very small except where action potentials from oxytocin cells were recorded, they can make no significant contribution to synchronizing the onsets of bursts in oxytocin cells that are not contiguous. 5. A standard antidromic stimulation from the pituitary stalk, at 40 Hz for 4 s, which stimulated both oxytocin neurones and vasopressin neurones, caused a delta[K+]o of 0.17-1.8 mM, the variation being mainly from rat to rat. The larger delta[K+]o values were accompanied by slow negative potentials of up to 1.5 mV, there was a gradient in delta[K+]o decreasing towards the pia at the inferior limit of the SON, and there was a slow increase in [K+] in the subarachnoid space.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Extracellular K+ in the supraoptic nucleus of the rat during reflex bursting activity by oxytocin neurones. 189 42

The mechanical properties of the longitudinal and circular muscle tissues of the human umbilical vein and the effects of nicardipine were investigated. Spontaneous contractions were observed in the isometric condition. When high concentrations of potassium (118mM-K+), oxytocin and serotonin were applied, these substances evoked contractions. Oxytocin (10(-4)-10(-2) U/ml) enhanced the spontaneous contractions. Serotonin produced contractions at 10(-9)-10(-4) M in both the longitudinal and circular muscle strips. When nicardipine (10(-5) M) was applied, contractions induced by 118mM-K+ were completely inhibited, but contractions induced by serotonin could not be completely abolished, i.e., tonic contractions ceased but small phasic contractions continued. Nicardipine (10(-8) M) did not inhibit the amplitude and frequency of spontaneous contractions, but decreased the basal tonus. These results suggested that nicardipine might improve feto-placental blood flow while decreasing the spontaneous basal tonus.
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PMID:Effect of vasoconstrictor and vasodilator on isolated human umbilical vein. 191 87

The effects of EtOH on peptide release and on high-threshold, voltage-activated calcium (Ca++) channels were examined in acutely dissociated rat neurohypophysial terminals. These terminals release the peptide hormones, arginine vasopressin (AVP) and oxytocin. Release of AVP from isolated intact neurohypophyses, induced by either electrical stimulation or elevated potassium, was inhibited by clinically relevant concentrations of EtOH. "Whole-cell" patch-clamp recording methods were used to study the effects of EtOH on voltage-activated Ca++ currents (ICa) in the peptidergic nerve terminals. Amplitudes of both fast-inactivating ICa and long-lasting ICa were reduced in EtOH, and the reduction in ICa did not result from a shift in its current-voltage or steady-state inactivation relationships. Only the fast-inactivating component recovered after removal of EtOH. The effects of EtOH on ICa could not be attributed to changes in osmolarity. In contrast to ICa, the fast, transient K+ current was insensitive to EtOH. These results suggest that EtOH-induced reduction of ICa in the peptidergic nerve terminals produces a decrease in AVP release, resulting in lowered plasma AVP levels.
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PMID:Calcium currents and peptide release from neurohypophysial terminals are inhibited by ethanol. 194 19

1. Magnocellular neuroendocrine cells (MNCs) in the supraoptic nucleus (SON) of mammals synthesize vasopressin or oxytocin and release these hormones systemically from their neurohypophysial axon terminals. In the rat, release is facilitated by bursts of action potentials generated by the MNC. However MNC units in the intact cat discharge more slowly and do not display the repetitive bursts (phasic firing) that promote vasopressin secretion. The reasons why these cat endocrine neurones differ so dramatically in their firing behaviour from the rat model were examined using intracellular recording. 2. Cat and rat MNCs displayed similar mean resting potentials approximating -60 mV, and were usually linear in their voltage-current relationship in the hyperpolarizing direction. However cat MNCs displayed a higher mean cell input resistance (301 M omega; n = 56) than those of rat (150 M omega; n = 105). 3. Calcium influx to cat MNCs during firing appeared comparable to rat based on (a) the similar range of action potential broadening observed during a spike train, (b) the shoulder on the action potential's falling phase which was blocked in low-Ca2+ saline, and (c) the ability to evoke tetrodotoxin (TTX)-insensitive spiking and non-synaptic depolarizing potentials, both calcium-mediated events observed in the rat. 4. In cat MNCs, a depolarizing current pulse (100-500 ms; 0.1-0.3 nA) elicited a train of action potentials followed by a prominent after-hyperpolarization (AHP) several times the duration of its counterpart in the rat. The AHP reversed near the equilibrium potential for K+, was not voltage dependent and represented an increased membrane conductance. It was suppressed in low-Ca2+ saline and completely eliminated by the calcium-activated potassium current (IK(Ca)) blockers apamin (100 nM) or d-tubocurarine (50-200 microM). Both blockers decreased spike frequency adaptation but did not induce bursting. Therefore the cat AHP probably represents a Ca(2+)-activated K+ conductance with a similar blocker sensitivity to its briefer counterpart in the rat MNC. 5. The spike hyperpolarizing after-potentials (HAPs) in cat were more than twice the mean amplitude and several times the duration of HAPs in rat. Cat HAPs were qualitatively similar to their rat counterparts, remaining unaffected by apamin or tubocurarine. The intrinsic currents responsible for the AHP and HAP appear to generate the stronger activity-dependent inhibition displayed by cat MNCs. 6. Twenty-one of fifty-two cat MNCs displayed an inward rectification at membrane potentials more negative than -70 mV ([K+]o = 6.24 mM), causing a depolarizing 'sag' in the voltage trajectory lasting 100-200 ms which was TTX resistant.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Intracellular study of calcium-related events in cat magnocellular neuroendocrine cells. 202 22

The influence of intrathecal injection of oxytocin (OT), anti-OT serum (AOTS) and naloxone on pain threshold and electroacupuncture (EA) analgesia in rats was investigated. The tail-flick induced by potassium iontophoresis was used to measure the pain threshold. The increase in pain threshold was observed within 70 min after OT injection (100 ng), and it was much more effective than that of the ACSF injection (P less than 0.001). The OT administration could enhance the EA analgesia. This effect was of dose-related. Although injection of AOTS did not affect the pain threshold, it diminished EA analgesia. Furthermore, injection of naloxone did not influence the action of OT on EA analgesia. Our results showed that OT in spinal cord plays an important role in the EA analgesia, and its effects is independent of endogenous opiate peptides.
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PMID:[Involvement of oxytocin in spinal cord in acupuncture analgesia]. 211 1

1. The ability of several potassium (K+) channel openers to inhibit spasm of the uterus of the nonpregnant rat and their susceptibility to antagonism by glibenclamide was assessed in vitro and in vivo. 2. In the isolated uterus exposed to oxytocin (0.2 nM), cromakalim, RP 49356 and pinacidil were of similar potency (mean pD2 = 6.4, 6.0 and 6.2 respectively) while minoxidil sulphate was of lower potency (pD2 = 4.7). Glibenclamide antagonized cromakalim and RP 49356 with the interactions consistent with competitive antagonism (mean pA2 of 6.57 and 7.00 respectively). Glibenclamide also antagonized pinacidil (pA2 = 6.22) but the slope of the Schild plot was significantly greater than -1. Neither salbutamol nor minoxidil sulphate was antagonized by glibenclamide (10 microM). 3. Cromakalim (1 and 10 microM), RP 49356 (1 and 10 microM), pinacidil (1 microM) and minoxidil sulphate (100 microM) suppressed spasm evoked by low (less than 40 mM) but not high (greater than or equal to 40 mM) KCl concentrations. Glibenclamide (10 microM) prevented cromakalim (10 microM)-, RP 49356 (10 microM)- and pinacidil (10 microM)-induced suppression of KCl (20 mM)-evoked spasm. Pinacidil (10 and 100 microM), cromakalim (100 microM) and salbutamol (0.01-1 microM) inhibited spasm evoked by all concentrations of KCl (10-80 mM). Suppression of spasm evoked by KCl (10-80 mM) by cromakalim (100 microM) and pinacidil (100 microM) was insensitive to glibenclamide (10 microM). 4. Cromakalim (0.1 mg kg-1) and RP 49356 (0.1 mg kg-1), given by i.v. bolus injection, inhibited uterine contractions, produced a fall in blood pressure and a slight tachycardia in the conscious ovariectomized rat. Glibenclamide (20mgkg-'), given by i.v. infusion, antagonized the vascular and uterine smooth muscle relaxant properties of cromakalim and RP 49356. 5. Several K+ channel openers are uterine relaxants. The antagonism of cromakalim, RP 49356 and pinacidil, at low concentrations, by glibenclamide suggests their actions may involve an ATP-sensitive K+channel. High concentrations of pinacidil (10 and 100 microM) and cromakalim (100 microM) may exert an additional action in the uterus. The low potency of minoxidil sulphate and its insensitivity to glibenclamide in the isolated uterus suggests that its mechanism of action may differ from that of the other K+ channel openers.
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PMID:Effects of several potassium channel openers and glibenclamide on the uterus of the rat. 212 95

The MP levels of the mammary gland's secretory cells and transepithelial differences of potential were found to depend on extracellular ions of sodium and chloride in lactating white mice. Substitution of the sodium ions with the choline ions increased a little the difference of potentials, whereas substitution of the chloride ions with sulfuric acid ions decreased it. Transepithelial electrical resistance increased in both cases. Substitution of the sodium ions with ions of choline and of the chloride ions with sulfuric acid ions suppressed hyperpolarization changes of the MP and increased the transepithelial difference of potentials. Contractile responses of myoepithelial cells to the action of acetylcholine and oxytocin were also depressed. The sodium and chloride ions seem to affect simultaneously the processes of the potassium ions release from secretory cells and contractile responses of the alveoli's myoepithelial cells.
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PMID:[The participation of sodium and chlorine ions in the reactions of the secretory cells and alveolar myoepithelium of the mammary gland]. 217 47

Incubation of neurointermediate lobes in Locke's solution containing 0.13 mumol.l-1 (6R)-5,6,7,8-tetrahydro-alpha-biopterin dihydrochloride (THB4) resulted in an inhibition of bioassayed vasopressin secretion and in an increase of that of oxytocin both under resting conditions as well as during depolarization due to excess potassium. It is suggested that some events related to THB4 and localized in the neural lobe are involved in the mechanism of vasopressin and oxytocin release.
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PMID:(6R)-5,6,7,8-tetrahydro-alpha-biopterin affects vasopressin and oxytocin release from rat neurointermediate lobe in vitro. 224 18

1. The effect of caffeine on mechanical activity was studied in pregnant rat myometrium. 2. In muscle cells with intact plasmalemmae, caffeine (0.1-50 mM) produced no contraction whatever the experimental conditions. 3. Caffeine (0.1-10 mM) inhibited, in a concentration-dependent manner, contractions induced by electrical stimulation, potassium-rich (60 mM K+) solution, sodium-free solution or oxytocin (22.5 nM). 4. In Ca2(+)-free solution, various substances (oxytocin, sodium orthovanadate and prostaglandin E2) evoked sustained contractions that were suppressed by caffeine (5-10 mM). When caffeine (greater than 5 mM) was applied during Ca2(+)-loading of the tissue (2.1 mM Ca2+, 5 min) in the presence of a K(+)-rich solution, the subsequent transient contraction induced by a short application (10s) of oxytocin (22.5 nM) in Ca-free solution was reduced (63 +/- 3.5% reduction for 20 mM caffeine, n = 4). 5. In saponin-skinned strips, application of caffeine (5-10 mM) during loading of the Ca2(+)-store increased the subsequent contraction induced by myo-inositol 1,4,5 trisphosphate (IP3, 10 microM). Caffeine (10-30 mM) decreased calcium-activated contractions in skinned fibres lacking a functional internal Ca-store. This effect was reduced by the cyclic AMP-dependent protein kinase inhibitor Thr-Thr-Tyr-Ala-Asp-Phe-Ile-Ala-Ser-Gly-Arg-Thr-Gly-Arg-Arg-Asn-Ala-Ile- His-Asp (8 microM). 6. In conclusion, it is suggested that the inability of caffeine to cause spasm of rat myometrium is due to the absence of a caffeine-sensitive calcium-release channel in the sarcoplasmic reticulum. Relaxant effects of caffeine can be explained by mechanisms leading to a decrease in both the cytoplasmic free Ca2+ concentration and the Ca2 +-sensitivity of the contractile machinery.
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PMID:Caffeine acting on pregnant rat myometrium: analysis of its relaxant action and its failure to release Ca2+ from intracellular stores. 232 93

It was found that 10(-8) mol/l oxytocin (OT) application exerted effects on functional properties of three types of acetylcholine (ACh) receptors in neurons identified in the ganglia of Helix pomatia under voltage clamp conditions. OT depressed ACh-induced sodium-potassium-calcium current in neuron RB3 without a shift of the reversion potential. The data obtained show that there are two types (subtypes) of ACh receptors connected with chloride channels. OT decreased the ACh-induced chloride current in neuron F4 and enhanced the ACh-induced chloride current and desensitization of ACh receptors in neurons D5, F86. Effects of OT and serotonin applications were reversible but not additional. Effects of OT injection and OT application were independent. The present results suggest that cyclic AMP may be the second messenger mediating the OT-induced modulation of functional properties of three types of ACh receptors.
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PMID:[Oxytocin modulation of the functional properties of 3 types of cholinoreceptors in mollusk neurons]. 233 36


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