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)

Direct measurements of cyclic AMP were performed in the isolated epithelium of frog skin. Phosphodiesterase inhibitors (methylxanthines, papaverine) and activators of adenylyl cyclase (oxytocin, catecholamines) significantly increased the cyclic AMP content. Propranolol completely blocked the generation of cAMP induced by beta-adrenergic agonists but had little or no effect on that induced by oxytocin. Phentolamine enhanced the cAMP production by adrenalin and noradrenalin. At supramaximal concentrations, oxytocin and isoproterenol produced similar increments in cAMP, while exposure to both agents roughly doubled the increase in cAMP. The results suggest the presence of independent receptors for oxytocin and catecholamines in frog skin, with additive effects on cAMP generation.
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PMID:Cyclic AMP levels in isolated frog skin epithelium: effects of phosphodiesterase inhibitors, oxytocin and catecholamines. 21 57

Isolated uteri from rats with regular 4-day cycles were incubated in Krebs-Ringer bicarbonate buffer and the release of PGF into the medium was measured by radioimmunoassay after extraction of the incubation medium with ethyl acetate at pH 3.0-3.5. PGF was produced from endogenous precursors and accumulated in equal amounts in the medium during two successive 60 min periods on each day of cycle, but the magnitude of the production varied significantly during the cycle, being greatest in estrus. Oxytocin in doses up to 500 mU/ml had no effect on PGF accumulation in the incubation period at any stage of the cycle, while epinephrine (10(-3)) greatly stimulated PGF release from the estrous uterus but had no effect on PGF release from the diestrous uterus. Phentolamine, an alpha-blocking agent, had no effect on the epinephrine-induced release of PGF, while propranolol, a beta-blocking agent, not only prevented in increase in PGF production induced by epinephrine but also reduced the basal release of PGF by the estrous uterus. Since oxytocin contracts and epinephrine relaxes the nonpregnant rat uterus both in vivo and in vitro, it is unlikely that the effects of these two compounds on uterine contractility are mediated by the release of PGF2alpha.
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PMID:Effects of epinephrine and oxytocin on the release of prostaglandin F from the rat uterus in vitro. 56 31

The effects of norepinephrine, phentalamine, oxytocin, vasopressin, several prostaglandins, and indomethacin on the spontaneous motility of isolated guinea pig cauda epididymidis were explored. Phentolamine and indomethacin reduced the isometric peak tension of spontaneous epididymal contractions. Phentolamine also depressed the frequency. Both findings suggest that catecholamines and endogenous prostaglandins are in some way regulators of the spontaneous motility of the cauda epididymidis. Norepinephrine resulted in the development of a distinct, sustained, tonic contraction without phasic activity, whereas prostaglandins E1, E2, and F2 alpha elicited a tonic increase accompanied by frequent, superimposed, phasic contractions. Both oxytocin and vasopressin comparably enhanced epididymal motility, producing contractile responses similar to those observed with prostaglandins. Since the epididymal contractions can influence the time spent by spermatozoa in passing through the ductus epididymidis, the above-mentioned compounds could play an important role in spermatozoal transport via modulation of epididymal contractile activity. In addition, such naturally occurring substances might regulate the release of sperm from the last portion of the epididymis into the ductus deferens.
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PMID:Physiologic and pharmacologic studies on the motility of isolated guinea pig cauda epididymidis. 80 41

The effects of intracerebroventricular infusions of naltrexone and phentolamine on the ability of vaginocervical stimulation to induce maternal behaviour, and plasma and cerebrospinal fluid (CSF) levels of oxytocin, were measured in oestrogen-primed ewes. Results showed that naltrexone, but not phentolamine, significantly inhibited maternal behaviour following vaginocervical stimulation. Naltrexone also prevented the CSF increase in oxytocin following vaginocervical stimulation but was without effect on plasma levels. Phentolamine did not prevent either CSF or plasma increases in oxytocin, following vaginocervical stimulation, but reduced basal plasma levels. Results are discussed in terms of an opioid influence on maternal behaviour which may be mediated through a modulation of central oxytocin release.
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PMID:Effects of intracerebroventricular infusions of naltrexone and phentolamine on central and peripheral oxytocin release and on maternal behaviour induced by vaginocervical stimulation in the ewe. 259 52

To test the hypothesis that functional postsynaptic alpha-2 adrenoceptors exist in rat myometrium, we examined whether specific binding sites for [3H]rauwolscine were present on microsomal membranes from myometrium of nonpregnant, day 16 pregnant and delivering rats and whether an alpha-2 adrenoceptor agonist has functional effects. The myometrium of rats at term undergoes a physiological denervation, confirmed in this study by ultrastructural examination of uterine samples and by [3H]saxitoxin binding studies. Binding sites for rauwolscine of similar Kd (11-15 nM) were present in all groups of myometrium and were localized on plasma membranes. There was no significant change in the density of rauwolscine binding sites in membranes from day 16 animals compared to nonpregnant ones, but a significant fall (38%) from these values at term. Strips of uterine circular or longitudinal muscle from nonpregnant, day-16 or day-22 pregnant rats failed to respond to the selective alpha-2 agonist, BHT-920, in the presence of propranolol; i.e., BHT-920 neither caused contraction nor inhibited contractions induced by oxytocin. BHT-920 did not affect the inhibitory effects of isoproterenol which were antagonized by propranolol. However, it antagonized contractions to norepinephrine in the presence of propranolol with a pKB value of 5.6 to 5.7. These contractions were phentolamine-sensitive. BHT-920 displaced rauwolscine from binding to all groups of myometria (IC50 = 2 to 3 x 10(-6) M) and displaced prazosin (Kd = 0.65 nM) from binding to myometria of nonpregnant rats (IC50 value congruent to 2 x 10(-4) M). Phentolamine also displaced rauwolscine from binding (IC50 = 2 x 10(-8) M). 5-Hydroxytryptamine displaced rauwolscine from binding only at higher concentrations (IC50 greater than 10(-5) M). We conclude that binding sites for alpha-2 adrenoceptor antagonists in myometrial microsomes were located primarily on smooth muscle plasma membrane. A smooth muscle alpha-2 adrenoceptor agonist appeared to occupy a site on muscle with the same affinity as it displayed toward rauwolscine binding site and competitively inhibited effects of an alpha-1 agonist. Our data suggest that alpha-2 adrenoceptor binding sites may exist on smooth muscle without coupling to contractile function, but their occupancy competitively prevents occupancy of alpha-1 agonist receptor activation sites.
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PMID:Alpha-2 adrenoceptors on nerves and muscles of rat uterus. 285 41

1. A search was made for an assay tissue with selective sensitivity to vasopressin. Of those smooth muscle preparations tested, the longitudinal muscle of the isolated rectum of the rabbit was the most satisfactory.2. The rabbit isolated rectum, bathed in Krebs solution, was contracted by acetylcholine, angiotensin II amide, bradykinin and 5-hydroxytryptamine. It was relaxed by vasopressin, oxytocin and the catecholamines.3. Vasopressin was active in concentrations of 4-100 muu./ml (0.01-0.25 ng/ml) and was 20-30 times more active than oxytocin. Bretylium had no effect on the relaxant action of vasopressin; nor did concentrations of alpha- and beta-adrenoceptor blocking agents sufficient to abolish the actions of catecholamines. Lignocaine reduced the sensitivity of the rabbit rectum to both vasopressin and oxytocin without altering the actions of adrenaline. High concentrations of either vasopressin or oxytocin desensitized the rabbit rectum to the actions of both hormones, without affecting the actions of adrenaline. It was concluded that vasopressin and oxytocin act on a common population of receptors different from those for catecholamines.4. Phentolamine, unlike other alpha-adrenoceptor antagonists, reduced the relaxant action of vasopressin on the rectum.5. When superfused with blood from an anaesthetized dog, the rabbit rectum maintained a higher tone than in Krebs solution; it retained its sensitivity to vasopressin. Pronethalol, administered intraluminally, reduced spontaneous movement and abolished the actions of low concentrations of catecholamines, thereby increasing the specificity of the assay. No other substance tested relaxed the rectum in concentrations likely to be found in blood.6. Vasopressin was stable in dog's blood; it survived passage through the pulmonary vascular bed; it had a half-life in the circulation of about 1 min.7. The half-life of vasopressin in the circulation may depend upon the duration of the infusion.
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PMID:A sensitive and specific assay for vasopressin in the circulating blood. 439 59