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)

1. Voltage-activated dihydropyridine-sensitive Ca2+ influx was measured in PC12 pheochromocytoma cells using 45Ca. 2. It has been found that oxytocin inhibits voltage-activated dihydropyridine-sensitive Ca2+ influx with ED50 about 0.30 x 10(-6) M. 3. Tolbutamide (1.3 x 10(-3) M) has no visible effect on both Ca2+ influx itself and on the inhibitory oxytocin effect. 4. External application of Li+ (10 mM) causes a slight shift of ED-curve to lower oxytocin concentrations. 5. It is suggested that the hydrolysis of phosphoinositides may play a role in oxytocin action on Ca2+ influx in PC12 cells.
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PMID:Inhibition by oxytocin of voltage-activated calcium influx in cultured PC12 pheochromocytoma cells. 171 91

We have investigated the action of tolbutamide and glibenclamide in a Ca-dependent process: the contractile activity of smooth muscle (uterus). The results obtained show that sulfonylureas are capable of relaxing contractions of rat uterus induced by various agents: oxytocin, acetylcholine and KCl in a medium with Ca2+. The capacity of sulfonylureas to also relax oxytocin-induced Ca-free contraction indicates the possibility that the action of these drugs could be due, above all, to a decrease in the intracellular free calcium level. Since maintained contraction induced by oxytocin in a Ca-free solution could be repeated after making a relaxation dose-response curve to sulfonylurea, the most likely mechanism of sulfonylurea-induced uterine relaxation is not an increase in the efflux of Ca but an increase in the Ca-uptake by intracellular organelles.
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PMID:Relaxant effects of sulfonylureas on induced contractions of rat uterine smooth muscle: role of intracellular calcium. 308 96

Depolarization of the neuronal membrane in the snail neurons induced by oxytocin application to the soma of these neurons have been examined under voltage clamp conditions. Replacement of external chloride by HEPES led to an increase its amplitude and a shift of its current-voltage characteristic in the depolarizing direction. External application of furosemide inhibited the current evoked by oxytocin application. Extracellular application of theophylline increased its amplitude. Imidazole, tolbutamide and temperature decrease had an opposite effect on this current. It is suggested that the surface membrane of some snail neurons probably possesses oxytocin receptors whose activation leads to the increase of its chloride permeability. This process is probably mediated through the system of cyclic nucleotides.
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PMID:[Effect of application of oxytocin on neurons of Helix pomatia: depolarization effects]. 321 Dec 30

Ionic mechanisms of hyperpolarization induced by oxytocin application on the neuronal membrane of identified neurons of Helix pomatia have been studied under voltage clamp conditions. There are two types of neurons and two types of hyperpolarization, respectively. Hyperpolarization of the first type is due to a decrease in chloride permeability and hyperpolarization of the second type is due to an increase in potassium permeability of the surface neuronal membrane. The reversion potential in the first case was -40 mV and decreased with addition of external solutions of furosemide or tolbutamide. The reversion potential in the second case was -70 mV, and with a 2-fold increase of external potassium concentration it shifted towards depolarization by 15 mV, while tolbutamide addition to the external solution induced no changes. It is supposed that Helix pomatia neurons have different receptors to oxytocin. Activation of some receptors causes a decrease in the membrane permeability for chloride ions, probably, through the system of cyclic nucleotides, while activation of their receptors increases potassium permeability of the surface membrane.
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PMID:[Effect of application of oxytocin on neurons of Helix pomatia: hyperpolarization effects]. 321 Dec 31

The in vitro spontaneous isometric-developed tension (IDT) of uterine horns obtained from diestrous rats exhibited, after 60 min of post-isolation activity, a clear decrease in magnitude, averaging 18.2 +/- 5.2%. In presence of tolbutamide, a concentration-dependent decrease of IDT, significantly greater than the spontaneous reduction (75.1 +/- 5.4%, with tolbutamide at 10(-4) M), was observed. Incubation with propranolol (10(-6) M) or with sotalol (10(-4) M) failed to alter the negative inotropism evoked by tolbutamide. On the other hand, the sulfonylurea (10(-4) M) shifted most points of the dose-response curve to the right for the contractile stimulation elicited by oxytocin, an influence not altered by the simultaneous presence of propranolol or sotalol. Tolbutamide failed to influence the negative inotropic dose-response curve for isoproterenol and did not modify the decrease in contractions evoked by theophylline (10(-4) M). It was also found that tolbutamide was devoid of action on the basal release of prostaglandin E2 from uterine strips and on the positive inotropic dose-response curve for added PGE2 or PGF2 alpha, constructed in presence of indomethacin (5 X 10(-6) M). The present findings do not permit a simple explanation regarding possible factors underlying the negative uterine inotropic influence of tolbutamide in the rat uterus. However, it appears that alterations in the integrity of tissue excitability and contractile apparatus, adrenergic implications, changes in uterine cAMP levels, inhibition of cyclo-oxygenase or low PEG2 synthesis and release, are not plausible mechanisms to explain the negative inotropism of tolbutamide. Therefore, it is suggested that the contractile depression evoked by tolbutamide and its action on the contractile effect of oxytocin might be linked to the impaired synthesis of other prostanoids, namely PGF2 alpha, PGI2 or PGD2, although the participation of not yet determined factor(s), namely changes in Ca2+ ion movements, cannot be discarded.
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PMID:Tolbutamide in vitro diminishes spontaneous and oxytocin-induced contractions of uterine smooth muscle from diestrous rats. 348 42

The present experiments were undertaken to examine whether leptin affects the electrical activity of neurones in the supraoptic nucleus (SON) by using brain slice preparation of male Wistar and obese Zucker rats. Bath application of leptin (10(-8) - 10(-12) M) induced mainly inhibitory response in SON neurones of Wistar rats, although a minority showed excitation. These effects were observed in both continuously and phasically active cells. The inhibitory effect of leptin still persisted in low Ca(2+), high Mg(2+) medium. Bath application of tolbutamide, which is known to inhibit ATP-sensitive potassium channel activity, did not reverse the inhibitory effect of leptin on SON neurones. The effect of bath application of leptin was also tested in SON neurones of obese Zucker rats. Although leptin still affected the electrical activity of some SON neurones of Zucker rats, the proportion of unaffected neurones was significantly higher than in Wistar rats. The results suggest that leptin may inhibit the secretion of both oxytocin and vasopressin by inhibiting the electrical activity of neurones in the SON via direct action. This inhibitory effect of leptin may be exerted through mechanisms other than activation of ATP-sensitive potassium channels.
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PMID:Leptin affects the electrical activity of neurones in the hypothalamic supraoptic nucleus. 1192 77