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

Toad urinary bladders were mounted in Ussing-type chambers and volt-age-clamped. At nonzero voltages only, small fluctuations in current, delta I, and therefore in tissue conductance, delta Gt, were detected. These fluctuations were caused by the smooth muscle of the underlying tissue which could be monitored continuously and simultaneously with the current, I. Inhibition of the smooth muscle contraction with verapamil (2 X 10(-5) M) abolished the fluctuations in I and Gt. Amiloride (10(-4) M) had no significant effect on the magnitude of delta Gt, oxytocin increased Gt without affecting delta Gt, and mucosal hypertonicity produced by mannitol increased delta Gt. These results are consistent with the hypothesis that two parallel pathways exist for passive current flow across the toad urinary bladder: one, the cellular pathway, was not affected by smooth muscle activity; the other, the paracellular pathway, was the route whose conductance was altered by the action of the smooth muscle. Thus the relationship between the cellular and shunt conductances of the epithelium of the toad urinary bladder, under a variety of conditions, can be investigated by utilizing the effects of the movement of the smooth muscle.
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PMID:Cellular and shunt conductances of toad bladder epithelium. 11 Sep 41

Experimental conditions are described in which transient and positive current responses across isolated frog skin epithelia can be elicited by sudden addition of Na and Li ions (2--40 mM) in the outer bathing solutions. Subsequent return to outer Na (or Li) free conditions produce similar transient current changes but in the opposite direction. Analysis of the curve responses shows that the transient component of each curve is best described by a single, fast exponential term equation in case of Na addition to preparation unpoisonned with ouabain. In contrast, an equation including two exponential terms (a fast and a slow one) is required to fit the curve responses observed across ouabain treated epithelia or if Li is added outside. The transient responses were not significantly altered by substituying Cl for SO4(2)-anions. They were completely prevented by Amiloride (5-10(-5) M), increased by oxytocin (20 mU/ml) and markedly dependent upon the outer Na concentration. Interpreted in term of compartmental analysis, these observations suggest that a) the frog skin epithelium contains 2 separated but communicating compartments having different degrees of accessibility from outside; b) only that compartment filling at a fast rate (0.5 min) is involved in the transepithelial Na transport; c) the other one, filling at a rate of 4 to 7 min, is resplenished only under conditions where the basal pump system has a reduced activity. Tentative localization of these compartment is proposed.
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PMID:Transient current changes and Na compartimentalization in frog skin epithelium. 108 78

1. The modification of the contraction of the rat testicular capsule to oxytocin (OT) by vanadate (0.7, 7 and 70 microM), ouabain (0.1 mM), and amiloride (10 microM to 1 mM) have been studied. 2. OT (1 nM-6 microM) and vanadate (10 microM-3 mM) induced contraction of the rat testicular capsule in a dose-dependent way (ED50: 188 +/- 66 nM and 82.8 +/- 7.4 microM, respectively). 3. Vanadate (0.7, 7 and 70 microM) and ouabain (0.1 mM) increases the contractile effect of OT (50 and 200 nM). 4. Amiloride (10 microM-1 mM) inhibit, in a dose-dependent way, the OT-contraction. 5. Amiloride (10 microM or 50 microM) block the ouabain but not the vanadate potentiation to OT.
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PMID:Effects of vanadate, ouabain and amiloride on the contraction of the rat testicular capsule to oxytocin. 193 5

1. Diphenylamine-2-carboxylate (DPC), added to the mucosal side of the frog skin, increased reversibly the short-circuit current (I0), even in SO2-(4) Ringer. Amiloride blocked this effect. 2. The maximal stimulation was 140% of the control value and the EC50 was 0.26 mM DPC. 3. The stimulatory effect of DPC was additive to that of oxytocin. 4. The dose-response curves for amiloride determined in the absence and in the presence of 1 mM DPC showed an IC50 of 1.0 microM and 0.8 microM amiloride, respectively. 5. Thus DPC, a blocker of Cl- channels in various Cl-transporting epithelia, exerts a stimulatory effect on the amiloride-sensitive Na+ transport in frog skin.
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PMID:Diphenylamine-2-carboxylate stimulates sodium ion transport in frog skin epithelium. 257 51

This paper presents a study of the action of phenobarbital (anticonvulsant barbituric acid with pK1 = 7.3 and pK2 = 11.8) on the short-circuit current and on the transepithelial conductance of the frog isolated skin. An increase in these parameters was found after addition of the drug to the outside medium (apical). This effect is significantly higher at pHs lower than pK1, suggesting that the neutral form of this substance is the active form. All studies were performed at pH 7. Phenobarbital induces a depolarization of the apical barrier and an increase in 22Na+ radioactive tracer fluxes, which parallel the increase in the observed short-circuit current. This suggests an opening of the Na+ channels in this barrier. A dose-response curve shows that phenobarbital possibly acts on two different sites, with different affinity constants and stoichiometries. To further characterize these channels, comparative studies with oxytocin (a hormone that opens amiloride-sensitive Na+ channels in the apical side) were performed. The results show that phenobarbital causes the same percentage of increase in Isc in control and oxytocin-pretreated skins. Amiloride was also found to inhibit the phenobarbital-sensitive channels with an affinity constant [KAMIL = (60 +/- 1.78) x 10(-8) M] insensitive to the phenobarbital concentration.
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PMID:Opening of frog skin sodium channels by phenobarbital. 789 87

We investigated the importance of changes in intracellular Ca(2+) concentration ([Ca(2+)](i)) for amiloride-sensitive alveolar fluid clearance (AFC) in late-gestational guinea pigs. Fetal guinea pigs of 61, 68, and 69 days (term) gestation were investigated under normal conditions and after oxytocin-induced preterm labor. AFC or alveolar fluid secretion was measured using an impermeable tracer technique. At 61 days gestation there was net secretion of fluid into the lungs, and at birth the lungs cleared 49 +/- 7% of the instilled fluid volume over 1 h. Induction of preterm labor with oxytocin induced AFC at 61 days gestation. When present, AFC was inhibited or reversed to net fluid secretion by amiloride (10(-3) M). Inhibition of membrane Ca(2+) channels by verapamil (10(-4) M) or depletion of intracellular Ca(2+) by thapsigargin (10(-5) M) reduced AFC when net AFC was evident. Amiloride lacked an inhibitory effect on AFC when instilled with verapamil or thapsigargin. The results indicate that AFC via amiloride-sensitive pathways develops during late gestation, and that inducing preterm labor precociously may activate such pathways. Our results suggest that Ca(2+) may act as a second messenger in mediating catecholamine-stimulated AFC.
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PMID:Ca(2+)-dependent stimulation of alveolar fluid clearance in near-term fetal guinea pigs. 1188 Feb 88

A possible natriuretic mechanism of action of oxytocin was investigated in male Sprague-Dawley rats. The effects of an intravenous bolus injection of amiloride on urine volume, potassium and sodium excretion, and osmolality were measured with and without an intravenous infusion of oxytocin in saline. Control values were obtained during the infusion of saline. Amiloride administered during an oxytocin infusion increased sodium excretion from 0.1 +/- 0.0 to 16.6 +/- 2.1 micromol/min. In animals treated with amiloride only, the sodium excretion was 4.5 +/- 0.8 micromol/min. The administration of oxytocin only resulted in a sodium excretion of 1.2 +/- 0.3 micromol/min. After the administration of oxytocin, amiloride increased urinary flow from 4.3 +/- 0.6 microl/min to 48.8 +/- 6.1 microl/min. In animals treated with amiloride only, the flow after the bolus dose was 17.7 +/- 1.8 microl/min. The administration of oxytocin only resulted in a flow of 8.5 +/- 1.6 microl/min. The amiloride-caused change in potassium excretion was not inhibited by oxytocin. In summary, the effects of amiloride were not inhibited by the actions of oxytocin. Amiloride administrated after reaching a near steady-state effect of oxytocin was found to give rise to an effect far greater than that after the administration of oxytocin or amiloride alone. It is concluded that the intrarenal natriuretic mechanisms of oxytocin do not emanate from the amiloride-sensitive sodium channels.
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PMID:The effect of amiloride during infusion of oxytocin in male sprague-dawley rats: a study of a possible intrarenal target site for oxytocin. 1829 70