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)

Substitution of the amino acid glycine for 7-proline in oxytocin produces an analog, [7-glycine]oxygocin, having markedly reduced antidiuretic and vasopressor activities but retaining considerable natriuretic activity. We administered this analog alone and with distally acting diuretic agents to test the hypothesis that oxytocin and its analogs decrease proximal tubular fluid reabsorption. If [7-glycine]oxytocin shares a common mechanism of action with any of these agents, the response to combined treatment should be less than additive, otherwise, the saluretic effect of both agents should be maintained. Subcutaneous administration of [7-glycine]oxytocin, 10 micrograms/kg, to conscious fluid-loaded rats produced a natriuresis, diuresis and kaliuresis. Hydrochlorothiazide and [7-glycine]oxytocin administered together to the same rats had a greater than additive effect on urine volume and sodium excretion. Furosemide and [7-glycine]oxytocin had an additive effect on urine volume, sodium and chloride excretion. Triamterene blocked the kaliuresis caused by [7-glycine]oxytocin, although the two agents administered together had a greater than additive effect on sodium excretion. These results indicate that [7-glycine]oxytocin does not share a common natriuretic mechanism or site of action with the above diuretics. Our data are consistent with the hypothesis that oxytocin and its analogs may increase urinary sodium excretion by decreasing net proximal tubular fluid reabsorption.
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PMID:Natriuretic effect of [7-glycine]oxytocin in the presence of diuretic agents in conscious rats. 735 43

Oxytocin-induced contractions of isolated strips of oestradiol-treated rat myometrium were found to be affected by exposure to the diuretic frusemide. At a concentration of 20 microM. frusemide transiently increased the force of contraction over a period of approximately 10 min. After this time there was a progressive fall in contractile force. At a higher concentration of 200 microM, only the progressive fall in force was seen until contractions were completely abolished. Frusemide has been reported to increase the activity of cAMP-phosphodiesterase in tissue extracts from oestradiol-treated rat myometrium. Therefore, the changes in contraction due to exposure to frusemide may be a reflection of the changes in intracellular cAMP resulting from a stimulation of cAMP-phosphodiesterase activity. In support of this idea, addition of dibutyryl cAMP was found to partially restore contractions after frusemide treatment. These data suggest that frusemide may be a useful tool in the manipulation of tissue cAMP levels in order to determine the different roles of cAMP in the oestradiol-treated rat myometrium.
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PMID:The effect of frusemide on oxytocin-induced contractions of the rat myometrium. 781 57

Furosemide increased the hydrosmotic water flow in the frog urinary bladder and promoted the ADH-like effect of inhibitors of phosphodiesterase cAMP, potentiated hydrosmotic effects of theophylline and serosal osmotic hypertonicity but failed to change the effect of pituitrin. Fur reversibly suppressed oxytocin-induced contractions in the rat myometrium, inhibited the activity of the frog urinary bladder PDE cAMP, whereas the activity of the enzyme from the rat medulla and myometrium was activated by saluretic. Incubation of the myometrium strips in Fur resulted in a decrease in the cAMP content of the tissue. The cAMP seems to play an important role both in the myometrium smooth muscle relaxation and in the oxytocin-activated contractions.
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PMID:[The mechanisms of the effect of furosemide on the water permeability of the frog bladder and on oxytocin-stimulated contractions of the rat uterus]. 816 67

Contractile responses induced by 25 mumol/l oxytocin in myometrial strips isolated from the uterus of estradiol-dominated rats comprised both phasic and tonic components. In a Ca(2+)-free medium (containing 0.1 mmol/l EGTA and no added Ca2+), the oxytocin-induced contractions seemed to be associated with Ca2+ release from intracellular stores. Frusemide, known to lower the cAMP level in the rat myometrium, did not affect the responses due to Ca2+ release but inhibited those mediated through an acceleration of the Ca2+ influx. The permanent presence of frusemide (1.5 mmol/l) in the CaCl2-containing medium influenced the oxytocin-induced responses in the same manner as did omission of Ca2+ from the medium. The frusemide-sensitive component of the responses to oxytocin was superimposed on a persistent contraction caused by KCl depolarization, suggesting that frusemide completely inhibited the oxytocin-induced Ca2+ influx. At the same time, frusemide moderately (by only 34 +/- 7%) decreased the amplitude of the KCl-induced contracture. This decrease varied with the frusemide concentration, and could be partly prevented by addition of dibutyryl-cAMP; i.e. probably, it was mediated by an inhibition of voltage-gated Ca2+ influx due to a decrease in the intracellular cAMP level. The data presented seem to suggest that in the rat myometrium exposed to oxytocin (25 mumol/l) both voltage-gated and receptor-operated Ca2+ entries are regulated by cAMP-dependent protein kinases.
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PMID:The inhibitory effects of frusemide on Ca2+ influx pathways associated with oxytocin-induced contractions of rat myometrium. 878 42