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)

Under continuous IV infusion of oxytocin, milk leakage was elicited in 6 lactating cows with full udders by induction of a vacuum (-30 cm of water) around 1 mammary papilla (teat) with a plethysmographic apparatus. The volumes of milk loss were measured every minute. Epinephrine injected either into the jugular vein (20, 100, and 500 micrograms) or into the external pudic artery (1.5, 7.5, and 37.5 micrograms) induced an increase in milk leakage in 5 cows. This effect could be antagonized by the beta-blocking agent sotalol hydrochloride (0.5 to 4 mg) injected into the external pudic artery. In 1 cow, however, epinephrine given intra-arterially exerted a biphasic effect, small doses inducing stimulation, and large doses evoking inhibition of milk loss. The stimulating effects were blocked by sotalol (2 mg). The inhibiting effects were antagonized by the alpha-blocking agent prazosin (2 mg).
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PMID:Action of epinephrine on the function of the teat sphincter in the lactating cow. 649 12

The investigation was carried out to observe the influence of stress upon the motility of the uterus from 1st to 5th day after parturition or cesarotomy. The experiments involved 24 lowland black and white cows; in 12 of them cesarean section was performed. The motility of the uterus was recorded with the balloon method by way of air transmission. The starting uterine contractions curve having been recorded, for 15-20 minutes one of following stress agents was applied: taking the calf away, change of stall, putting under restraint, collecting small amounts of blood or milking by a strange person. Besides, 2 ml 0.1% adrenaline solution or 4 I.U. oxytocin was administered intravenously. Adrenaline was administered before or after oxytocin, or both the hormones were applied together. Oxytocin was also applied during the stress. During the action of the stress as well as after administration of adrenaline there was observed complete decay of uterine contractions from 1st to 5th day after parturition or cesarotomy. No changes in the motility of the uterus were brought about by intravenously administration of oxytocin during the stress. No response of the uterus to oxytocin was observed, either, when adrenaline had been administered before. Both exogenic and endogenic adrenaline was found to restrain strongly the contractions of the examined organ, or to decay them completely, which has a negative effect upon involution of the uterus in cows in the first days after parturition.
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PMID:[Effect of stress on uterine contraction in cows]. 730 31

In an in vitro trial on 80 pregnant and nonpregnant mice, the sensitivity of the uterus myometrium to the vasoconstrictors vasopressin, ornipressin, epinephrine, and norepinephrine was examined in comparison with oxytocin as a standardized stimulative drug. The pregnant uterus showed a significantly increased sensitivity to ornipressin, vasopressin, and norepinephrine. Epinephrine showed no uterus-stimulating effect, and an increase of sensitivity caused by pregnancy was not detected.
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PMID:Vasoconstrictors during pregnancy--in vitro trial on pregnant and nonpregnant mouse uterus. 789 Sep 95

Effect of various doses of oxytocin, vasopressin or adrenalin on the thyroid gland activity was studied in hypophysectomized and nonoperated rats 20 minutes after a single injection of the neurohormones. The minimal applied dose of the neurohormones stimulated increasing of their concentration in blood up to level typical for stress reaction. Injection of oxytocin led to no effect at any dose. In nonoperated rats vasopressin stimulated the thyroid gland but did not influence on TSH level in blood. In hypophysectomized rats thyrostimulating effect of vasopressin was also detected need. Adrenalin injection inhibited the thyroid gland function in both nonoperated and hypophysectomized rats. Effect of adrenalin in combination with vasopressin was like the action of adrenalin alone. Thus, it is possible to assume that under stress conditions a high blood level of adrenalin attenuates thyrostimulating effect of vasopressin.
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PMID:[The blocking effect of adrenaline on the thyroid-stimulating effect of vasopressin in rats]. 804 87

Stageness in the protein glands development is influenced by the nervous system mediators. Adrenergic mediation was established not to be developed by the period of provisory differentiation and appears to grow weaker by senile age. Acetylcholine stimulates growth and proliferation in the form of layers and bands. Adrenalin exerts its influence on organotypical level, which manifestates in reservation of the specific differentiation and protein type functioning of the gland. Hypothalamic neurohormones (oxytocin, vasopressin) influence the maintainance of the secretory epithelium viability.
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PMID:[The morphofunctional characteristics of the epithelium of the salivary glands and the neuroendocrine regulation of its histogenesis]. 868 39

We studied the mechanisms underlying alpha2-adrenergic receptor (AR)-mediated increase in intracellular free calcium ([Ca2+]i) in freshly dispersed myometrial cells from sows in the luteal phase of the estrous cycle. After the blockade of beta-ARs with propranolol, epinephrine increased [Ca2+]i dose-dependently in both the presence and absence of extracellular Ca2+. The rank order of alpha antagonists in inhibiting [Ca2+]i response to epinephrine was yohimbine > WB4101 >> prazosin in both the presence and absence of extracellular Ca2+, suggesting that epinephrine acts on alpha(2A)-ARs to increase Ca2+ influx as well as Ca2+ release from intracellular stores. Thapsigargin, the blocker of the Ca2+ pump in the sarcoplasmic reticulum, abolished the release but did not affect the influx. Pertussis toxin (PTX) inhibited the influx but failed to change the release. Nimodipine, an L-type Ca2+ channel blocker, nearly abolished the influx. The peak increase in [Ca2+]i caused by epinephrine was reached within 20 sec of administration. Intracellular cAMP concentrations were also decreased at 20 sec post-epinephrine. Epinephrine enhanced the L-type Ca2+ channel current, whereas forskolin suppressed it. Maximization of intracellular cAMP content by applying 8-bromo-cAMP (100 microM) blocked the effect of epinephrine on the current. U-73122, a phospholipase C inhibitor, reduced the Ca2+ release by epinephrine and oxytocin. Our results suggested that 1) activation of alpha2-ARs induces Ca2+ influx through opening L-type Ca2+ channels as well as inducing Ca2+ release from intracellular stores, and 2) a PTX-sensitive G protein couples negatively to adenylyl cyclase, leading to a decrease in cAMP formation which may be involved in the activation of Ca2+ channels. In addition, our results are consistent with the coupling of alpha2-ARs to a PTX-insensitive G protein (G(q)) to release Ca2+ from intracellular stores.
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PMID:Alpha2-adrenergic receptor-mediated Ca2+ influx and release in porcine myometrial cells. 916 Jul 37

We examined possible mechanisms underlying seasonal stress modulation in Lapland longspurs (Calcarius lapponicus), a species that breeds and molts (the energetically costly replacement of feathers) in the Alaskan Arctic. Free-living Lapland longspurs show dramatically reduced maximal corticosterone release during molt compared with the breeding season, an effect lost in captive birds. Neither changes in corticosterone binding proteins nor the overall condition of the bird (assessed by weight and fat storage) can explain different seasonal corticosterone responses. Adrenal insensitivity also does not fully explain reduced maximal output because exogenous ACTH enhanced corticosterone release during molt. Exogenous ACTH in molting birds, however, cannot stimulate corticosterone to stress-induced levels during breeding, implying reduced adrenal capacity. Lapland longspur pituitaries appeared to respond to exogenous corticotropin-releasing factor, arginine vasotocin, and mesotocin (the avian equivalents of arginine vasopressin and oxytocin) during molt, suggesting that a mechanism upstream of the pituitary blunts corticosterone release. Taken together, these results indicate that seasonal modulation of corticosterone release in this species is controlled at multiple sites in the hypothalamic-pituitary-adrenal axis.
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PMID:Hypothalamic-pituitary-adrenal axis changes allow seasonal modulation of corticosterone in a bird. 961

The neuropeptides angiotensin II (AngII) and oxytocin (OT) play important but opposing roles in the regulation of sodium appetite in the rat, AngII as a stimulatory peptide and OT as an inhibitory peptide. Adrenal steroids increase the density of AngII receptors in brain following in vivo administration, although the neuroanatomical and subtype specificity have not been thoroughly examined. Furthermore, previous studies demonstrate that adrenalectomy (ADX) leads to a reduction in OT receptors, although regions associated with sodium appetite remain to be examined. In the present study, quantitative receptor autoradiography was used to locate regions where perturbations in circulating adrenal steroids affect the density of oxytocin receptors and the angiotensin receptor subtypes AT1 and AT2. The results show that ADX results in a small, but significant decrease in AT1 expression in the paraventricular nucleus of the hypothalamus, subfornical organ, and the area postrema. That this effect is reversed by either aldosterone or low-dose corticosterone replacement suggests that occupancy of the mineralocorticoid receptor is responsible for the steroid effect. No changes were observed in AT2 or OT receptors in nuclei associated with sodium appetite, indicating that perturbations in adrenal steroids did not affect these receptors in brain regions implicated in the control of salt appetite.
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PMID:Adrenal steroid regulation of central angiotensin II receptor subtypes and oxytocin receptors in rat brain. 975 19

The influence of oxytocin, adrenalin and their combination on rat thyroid gland was studied after intraperitoneal administration of these hormones and following incubation of thyroid gland fragments in media, containing the neurohormones. Thyrostimulating effect of oxytocin (increase in thyrocyte height and 3H-leucine incorporation) was demonstrated in in vivo and in vitro experiments. Adrenaline did not cause morphofunctional changes in thyrocytes although it suppresses oxytocin thyrostimulating effect when administered simultaneously with it in both in vivo and in vitro experiments.
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PMID:[Morphofunctional characteristics of rat thyroid gland under the combined effect of oxytocin and adrenaline]. 1056 51

The effects of jugular infusions of adrenalin and the beta-adrenergic receptor antagonist propranolol on plasma concentrations of progesterone and oxytocin were examined at 2 different stages of the caprine estrous cycle. Adrenalin (25 micrograms.kg-1h-1) significantly (P < 0.05) increased oxytocin secretion on Day 3 and Day 10 of the cycle (estrus = Day 0); progesterone concentrations were significantly (P < 0.05) elevated on Day 10 alone. Propranolol had no effect on progesterone secretion yet significantly (P < 0.05) reduced oxytocin concentrations on Day 3. These results suggest that there may be neuroendocrine involvement in the regulation of luteal oxytocin secretion in the goat.
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PMID:Effect of adrenalin and propranolol on progesterone and oxytocin secretion in vivo during the caprine estrous cycle. 1073 92


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