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)

The contraction of the potassium depolarized pulmonary artery of the guinea pig was diminished by the calcium antagonists nifedipine, gallopamil, diltiazem, verapamil and prenylamine. The drugs are listed here in order of activity. The uptake of 45Ca of the depolarized pulmonary artery was reduced by nifedipine, verapamil and prenylamine in this order of activity. The depression of the coronary flow of the isolated guinea pig heart, which was brought about by barium chloride, antigenic rabbit serum or vasopressin plus oxytocin was reduced by infusion of prenylamine. The positive inotropic effect of K-strophanthin on the isolated, electrically stimulated left atrium of the guinea pig heart was reduced by gallopamil, verapamil, prenylamine, diltiazem and nifedipine in this order of activity.
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PMID:Effects of calcium antagonists on coronary spasm and pulmonary artery contraction in comparison to their antagonistic action against K-strophanthin in isolated guinea pig atria. 710 Feb 59

In order to obtain evidence for a central release of vasopressin and oxytocin, the release of these peptides was demonstrated in various extrahypothalamic areas of the rat brain. It proved that in those areas where these peptidergic fibers terminate synaptically a vasopressin and/or oxytocin calcium-dependent release, similar to that in the neurohypophysis, could be evoked by potassium or veratridine. Such release was not found in areas in which these fibers do not exhibit synaptic specialization.
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PMID:Vasopressin and oxytocin release in the brain--a synaptic event. 717 22

1. The action of vasoactive intestinal peptide (VIP) on the electrical and mechanical activity of strips of longitudinal myometrial smooth muscle from rabbits and guinea-pigs treated with oestradiol was studied in the sucrose-gap apparatus. 2. In myometrial strips which spontaneously exhibited regular contractions, or which were induced to contract rhythmically to the application of oxytocin, VIP reduced both the frequency and the force of contraction. 3. Contractions were associated with bursts of action potential discharge. In guinea-pig, the membrane potential reached its most negative value shortly following a burst and a slow decay of negativity followed ("generator potential'). VIP inhibited the decay of this negativity and increased the duration of the period between bursts. In rabbit myometrical strips, electrical discharges occurred less regularly but VIP also had an inhibitory action. The inhibitory action of VIP was not affected by the beta-adrenoreceptor blocker propranolol, by tetrodotoxin, or by apamin. 4. Using the double sucrose-gap apparatus, bursts of action potentials and contractions were elicited with depolarizing electrical pulses in the absence of oxytocin. Changes in membrane resistance were also estimated by eliciting hyperpolarizing electrotronic potentials. VIP hyperpolarized the membrane and inhibited contractions as depolarizing pulses now failed to reach threshold for action potential discharge or fewer action potentials were discharged. A small (about 10%) reduction in membrane resistance was freqeuently observed during the hyperpolarization. 5. If a single action potential was elicited in the presence of VIP, the tension generated by the muscle was less than in its absence. 6. In a calcium-free high-potassium (126 mM) solution, readmitting calcium produced contraction; VIP inhibited this contraction. Activation of beta-receptors by means of isoprenaline had a similar effect but unlike isoprenaline the action of VIP was not blocked by propranolol. 7. It is suggested that the primary action of VIP is on the calcium economy of the myometrial smooth muscle cell, possibly to accelerate sequestration and/or extrusion of calcium from the cell. In some way this is associated with inhibition of the generator potential, hyperpolarization, and with a small increase in permeability of the membrane to potassium.
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PMID:Mechanism of action of vasoactive intestinal polypeptide on myometrial smooth muscle of rabbit and guinea-pig. 732 Aug 97

1 The effect of oxytocin was studied on the isolated vas deferens of the rat. 2 Oxytocin (25 to 200 mu/ml) reversibly reduced the contractile response induced by noradrenaline, dopamine and acetylcholine. 3 Oxytocin (400 mu/ml) abolished the response to potassium. 4 The contractions evoked in the vas deferens by field stimulation were also reduced by oxytocin (50 to 200 mg/ml). The inhibitory effect of the drug was related to the external calcium concentration. 5 It is suggested that oxytocin depresses the contractile responses in the vas deferens at least partly by reducing the availability of calcium from an extracellular source.
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PMID:Effects of oxytocin on the isolated vas deferens of the rat. 739 48

Previous studies had failed to observe cromakalim-induced 42K+ or 86Rb+ efflux from the myometrium of the pregnant rat in contrast to positive findings in other smooth muscles. In the current study, in myometrium from the non-pregnant rat, cromakalim (10 microM) and RP 49356 ([(+/-)-N-methyl-2-(3-pyridyl)-tetrahydrothiopyran-2-carbothioamid e-1-oxide); 10 microM) induced small increases in 42K+ or 86Rb+ efflux but much less than did oxytocin (20 nM) or KCl (20 mM). The cromakalim-induced increase in 42K+ efflux was enhanced 3.5-fold in the presence of KCl (20 mM) plus (+)-cis-diltiazem (3 microM), a property shared by RP 49356. Glibenclamide (10 microM) partially reduced the cromakalim-induced 42K+ efflux, in the presence of KCl and (+)-cis-diltiazem, but did not affect the KCl-induced 42K+ efflux. The data provides further support for the idea that cromakalim and RP 49356 are able to open potassium channels in rat myometrium. It would appear that their actions in this tissue are dependent on the extracellular K+ concentration and/or membrane potential.
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PMID:Cromakalim- and RP 49356-induced 42K+ and 86Rb+ efflux in rat myometrium. 749 97

Thimerosal inhibits calcium uptake and IP3-induced calcium release from IP3-sensitive endoplasmic reticulum; this study sought to evaluate the effects of thimerosal on agonist-stimulated phasic myometrial contractions. Thimerosal was found to significantly inhibit phasic contractions stimulated by oxytocin, aluminum fluoride, potassium chloride, ionomycin, and Bay K 8644. These observations provide support for the hypothesis that calcium uptake and IP3-induced calcium release are important events during agonist-stimulated phasic myometrial contractions.
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PMID:The effects of thimerosal, a sulfhydryl reagent, on phasic myometrial contractions. 753 99

These studies sought to test the hypothesis that potassium-stimulated phasic myometrial contractions utilize cytosolic calcium oscillation-like mechanisms comparable to those activated in response to oxytocin. Uterine tissue was obtained from pro-oestrus/oestrus Sprague-Dawley rats. In vitro isometric contraction studies were performed using longitudinal myometrial strips; computer digitalized contraction data were analyzed for contraction area, and normalized for tissue cross-section area. Dose-response studies were performed using potassium chloride with and without inhibitors of cytosolic calcium oscillation mechanisms. Qualitative inositol-phosphate production studies were performed after preloading uterine tissue with [3H]inositol; subsequently, the individual inositol-phosphates produced in response to stimulation were isolated by anion exchange chromatography. Potassium chloride over a concentration of 10 to 30 mM produced a dose-related increase in phasic contractile activity. The potassium-stimulated phasic contractions were significantly suppressed in response to inhibition of phospholipase C, stimulation of protein kinase C, inhibition of calcium-induced calcium release, and prevention of extracellular calcium influx. The qualitative inositol-phosphate production studies confirmed activation of phospholipase C in response to 20 mM potassium. These studies have provided support for the hypothesis that potassium-stimulated phasic myometrial contractions activate intracellular signal transduction mechanisms comparable to those activated in response to hormonal uterotonic agonists.
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PMID:Potassium chloride effects on the hormonal signal transduction mechanisms underlying phasic myometrial contractions. 759 44

Intravenous infusion of oxytocin (OT) (10-100 nmol/kg/30 min) to 8-week-old anesthetized male rats resulted in a dose-dependent increase in urine volume, which showed a peak value 30-45 min after the start of OT-infusion. Urinary excretions of sodium, chloride and potassium were also increased by OT, showing peak values at 30-45 min, without any increase in the creatinine level. The natriuresis by OT was accompanied by increased excretion of urinary active kallikrein, which showed a peak value 15 min after the start of OT-infusion. The urinary kinin level was also increased. Intravenous infusion of a kallikrein inhibitor, aprotinin (15 mg/kg/90 min), when started 30 min before the OT-infusion, significantly inhibited the OT-induced increase in urine volume and urinary excretion of sodium, chloride and potassium. Intravenous infusion of a bradykinin B2 antagonist, Hoe 140 (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]BK, 4.5 mg/kg/90 min), when started 30 min before the OT-infusion, significantly inhibited the OT-induced increases in urine volume and urinary excretion of sodium and chloride, but not that of potassium. These results indicate that the OT-infusion induces natriuresis in male rats, and more than half of the natriuresis is mediated by a concomitant increase in excretion of urinary active kallikrein and the kinin generated.
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PMID:Oxytocin-induced natriuresis mediated by the renal kallikrein-kinin system in anesthetized male rats. 763 42

Sheep which were predominantly urinary excretors (U) or faecal excretors (F) of sodium were exposed to a 75% reduction of water intake for 72 h. The experiment was performed on moderate, low or high sodium intakes (0.4, 0.05 or 1.2 mmol kg-1 day-1) to test the hypothesis that dehydration natriuresis was not a cause of sodium depletion but a defence against hypernatraemia. Dehydration caused elevation of plasma sodium concentration, osmolality, antidiuretic hormone (ADH) and oxytocin but, as in other experiments, a fall in haematocrit. The two higher levels of sodium intake were associated with dehydration natriuresis but also a smaller increase in faecal sodium excretion in both U and F sheep. On low sodium intake, however, neither urinary nor faecal sodium excretion increased in either group of sheep although the rise in plasma sodium concentration caused by dehydration was similar. Thus, when there is a risk of sodium depletion, due to low sodium intake, dehydration natriuresis does not occur, consistent with the hypothesis. Active sodium transport inhibitor (ASTI) and atrial natriuretic peptide (ANP) fell rather than rose during dehydration. Since aldosterone is suppressed by the higher levels of sodium intake, none of these hormones is likely to mediate dehydration natriuresis in sheep. F sheep showed more effective renal and faecal water conservation when dehydrated. During water restriction, the urinary potassium excretion of U sheep was significantly reduced, unlike that of F sheep; moreover, the latter maintained an identical plasma potassium concentration between baseline and restriction period, whereas in U sheep it was 0.3 mmol l-1 higher during water restriction. Increased drinking rather than reduced urine output was the basis of rehydration when ad lib. water intake was restored.
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PMID:Responses to reduced water intake, including dehydration natriuresis, in sheep excreting sodium predominantly in urine or in faeces. 778 17

Morphological and pharmacological evidence suggest that the dense GABAergic innervation of the supraoptic nucleus is important for regulating the electrical activity of vasopressin and oxytocin neurons. We have employed the technique of intracranial microdialysis to examine extracellular GABA concentrations in the supraoptic nucleus of the anaesthetized rat and questioned whether differences exist in the dynamics of GABA release between virgin and lactating rats, and if events during lactation or following blood pressure manipulation alter endogenous GABA levels in this nucleus. No significant differences were detected between virgin and lactating animals in either basal or 100 mM potassium ion-evoked GABA release. The inclusion of the GABA uptake blocker nipecotic acid (0.5 mM) into the dialysate resulted in a six- to eight-fold increase (P < 0.01) in GABA outflow in both groups of animals. In lactating rats, GABA outflow measured at 4 min intervals was not altered during a 60 min period of suckling by a full litter of pups and no significant change in GABA outflow was detected in relation to individual milk ejections. In virgin rats, removal of 1.5-2 ml of blood resulted in a 30-60 mmHg fall in blood pressure and a non-significant decline in GABA outflow. Replacement of blood resulted in an abrupt 50 mmHg increase in blood pressure and a significant 22% increase in GABA outflow (P < 0.01), but no change in aspartate or methionine concentrations. Repeated intravenous injections of the alpha-adrenoceptor agonist, metaraminol, similarly evoked approximately 50 mmHg increments in blood pressure and a 26% increase in GABA outflow (P < 0.05). Electrical stimulation of the diagonal band of Broca for 10 min produced a two-fold increase in GABA outflow from the supraoptic nucleus (P < 0.05). These results show that the overall profile of basal and potassium-stimulated GABA concentrations in the supraoptic nucleus is not substantially different between lactating and virgin rats. In lactating animals we have found that GABA levels are not altered in response to suckling or at the time of high-frequency firing by oxytocin neurons to induce milk ejection. In contrast, our data further support the hypothesis that GABA inputs to supraoptic neurons are part of a baroreceptor reflex, relaying through the diagonal band of Broca, to signal periods of acute hypertension and inhibit the firing of vasopressin neurons. Such observations suggest the physiological importance of GABA inputs to the supraoptic nuclei and indicate that GABA may be used in a stimulus-specific manner to influence the activity of magnocellular neurons.
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PMID:Extracellular GABA concentrations in rat supraoptic nucleus during lactation and following haemodynamic changes: an in vivo microdialysis study. 789 64


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