Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intact cyclic ewes have been used in experiments designed to examine the mechanism by which uterine oxytocin receptor synthesis is controlled during the oestrous cyclic. Previous experiments have shown that the prostaglandin F2 alpha analogue cloprostenol is luteolytic in ewes receiving oxytocin by continuous intra-venous infusion. When ewes receiving oxytocin are given cloprostenol uterine oxytocin receptor concentrations are raised, whereas in animals receiving oxytocin alone, they remain low. To investigate whether inhibition of oxytocin receptor binding activity by oxytocin is either dependent on elevated plasma progesterone concentrations or over-ridden by oestrogens secreted by ovarian follicles maturing as a result of cloprostenol treatment, ewes were given oxytocin by continuous intravenous infusion (3 nmol h-1) between Days 12 and 17 after oestrus and one of the following: no further treatment; cloprostenol [125 micrograms intramuscularly (i.m.)] on Day 15; progesterone, by subcutaneous implant, from Day 14 with cloprostenol on Day 15; medroxyprogesterone acetate (MPA; 6 mg depot i.m.) on Day 14 followed by cloprostenol on Day 15; or oestradiol-17 beta (2.75 mumol i.m.) on Days 14 and 15. Concentrations of oxytocin receptor were measured at autopsy on Day 17 in caruncular endometrium, intercaruncular endometrium and myometrium. Ovarian follicles and corpora lutea were examined to determine the effect of treatment on these tissues. Treatment with oxytocin alone resulted in the maintenance of corpora lutea, reduced follicular development and a low concentration of uterine oxytocin receptor. Cloprostenol initiated luteolysis in oxytocin-treated ewes. This was associated with a high level of oxytocin receptor binding activity in all ewes except those receiving exogenous progesterone.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effect of continuous infusion of oxytocin on ovarian function and uterine oxytocin receptor concentration in the cyclic ewe. 133 7

The affinity of vascular vasopressin receptors was studied to determine its role in altered vascular contractile sensitivity in deoxycorticosterone acetate (DOCA)-salt hypertension. Ring segments of rat mesenteric arteries were used to study vascular vasopressin receptors. Male Wistar rats were given subcutaneous injections of DOCA and 1% NaCl in the drinking water. Mesenteric arteries from hypertensive rats had a reduced contractile sensitivity to arginine vasopressin (AVP) and lysine vasopressin (LVP). The order of potency of vasopressin receptor agonists (AVP greater than LVP greater than oxytocin) was the same in arteries from hypertensive compared with normotensive animals. The affinity of the vasopressin receptor antagonist [deamino-Pen1,O-Me-Tyr2,Arg8] vasopressin, and the affinities of the vasopressin receptor agonists AVP and LVP were not altered during developing DOCA-salt hypertension. There was no change in contractile sensitivity to norepinephrine and KCl in arteries from hypertensive rats. The reduced vasopressin contractile sensitivity is not due to a change in vasopressin receptor affinity but may be a compensatory response to elevated blood pressure. These data suggest that increased vascular sensitivity does not contribute to elevated blood pressure during the developing stage of DOCA-salt hypertension.
 ...
PMID:Reduced contractile sensitivity and vasopressin receptor affinity in DOCA-salt hypertension. 153 57

A series of experiements was performed to determine whether proteins produced by the sheep conceptus (oCSP) during the time of maternal recognition of pregnancy or bovine recombinant interferon alpha 1-1 (brIFN) decrease oxytocin receptor concentrations in the endometrium of cyclic or ovariectomized progesterone-treated ewes. In experiment 1, cyclic ewes received intrauterine infusions of serum proteins (oSP), oCSP or brIFN on days 12, 13 and 14 of the oestrous cycle. Ewes then received an oxytocin challenge (1 microgram in 0.9% NaCl), and blood samples were taken just before and every 10 min for 1 h after the challenge; these were measured for 13,14-dihydro-15-ketoprostaglandin F 2 alpha (PGFM), the stable metabolite of prostaglandin F 2 alpha. Endometrial oxytocin receptor concentrations were then measured. The oCSP and brIFN treatments suppressed both endometrial oxytocin receptor concentrations and oxytocin-induced increases in PGFM concentrations. In experiment 2, ewes were ovariectomized and then pretreated with a fluorogestone acetate-releasing intravaginal device for 10 days followed by oestradiol (25 micrograms i.m. twice daily for 2 days). Ewes were then treated with progesterone (10 mg i.m. twice daily for 12 days). Ewes received intrauterine infusions of oSP, oCSP and brIFN on days 10, 11 and 12 of progesterone treatment. On the day after the last progesterone treatment, ewes were challenged with oxytocin and blood samples collected to measure PGFM. Endometrial oxytocin receptors were also measured. Treatment with oCSP, but not brIFN, suppressed endometrial concentrations of oxytocin receptor, and neither oCSP nor brIFN altered oxytocin-induced increases in PGFM concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Ovine conceptus secretory proteins and bovine recombinant interferon alpha (1)-1 decrease endometrial oxytocin receptor concentrations in cyclic and progesterone-treated ovariectomized ewes. 166 51

The effects of the activation of protein kinase A (PKA), protein kinase C (PKC) and corticosteroids were investigated on the release of corticotrophin-releasing factor-41 (CRF), arginine vasopressin (AVP) and oxytocin from rat fetal hypothalamic cells in culture. Both forskolin and PMA (phorbol 12-myristate 13-acetate) increased CRF, AVP and oxytocin release, while dexamethasone and aldosterone only reduced basal secretion of CRF. Both steroids also inhibited forskolin-induced CRF, AVP and oxytocin responses to PMA. These data provide direct evidence for a role for both PKC- and PKA-mediated mechanisms in the regulation of CRF, AVP and oxytocin release and for differential effects of both glucocorticoids and mineralocorticoids on PKA- and PKC-stimulated responses.
 ...
PMID:Release of corticotrophin-releasing factor-41, arginine vasopressin and oxytocin from rat fetal hypothalamic cells in culture: response to activation of intracellular second messengers and to corticosteroids. 173 59

The contribution of protein kinase C to the contraction by oxytocin of rat uterine longitudinal smooth muscle in Ca(2+)-free solution was investigated. Immunological analysis revealed that type II (beta) and III (alpha) protein kinase C subspecies were present in rat uterine smooth muscle. The pretreatment of a diacylglycerol kinase inhibitor R59022 to accumulate diacylglycerol potentiated the Ca(2+)-independent contraction. The contractile activity was diminished with the depletion of protein kinase C, when the contraction was evoked repeatedly by oxytocin during the prolonged exposure to a tumor-promoting phorbol ester 12-O-tetradecanoylphorbol 13-acetate. These results suggested the involvement of protein kinase C in oxytocin-induced contraction in Ca(2+)-free solution.
 ...
PMID:Involvement of protein kinase C in Ca(2+)-independent contraction of rat uterine smooth muscle. 188 74

The synthesis and release of PRL are regulated by a variety of factors that originate in the hypothalamus, peripheral tissues, or posterior pituitary (PP). We recently reported that coculture of anterior pituitary (AP) and PP cells induced an increase in both PRL cell content and the responsiveness of lactotrophs to TRH. The aim of the present study was to determine whether the augmented response to TRH is due to increased lactotroph sensitivity to this particular secretagogue or to enhancement of the releasable pool of PRL. Cells obtained from anterior pituitaries of adult male rats were plated either alone or together with PP cells at the same total density. Cells cultures were maintained in serum-free medium for 4 days and then incubated for 20 min with the designated substances. Angiotensin-II and TRH evoked a significantly larger release of PRL in AP + PP cocultures than in AP cells cultured alone; the greatest difference between the culture types was observed at the highest concentrations of both secretagogues. The stimulation of PRL release by KCl, the calcium ionophore A23187, and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate was higher in the presence of PP cells than in cultures of AP cells alone, although the magnitude of this effect was lower than that seen with PRL secretagogues. The concomitant application of A23187 and 12-O-tetradecanoylphorbol-13-acetate resulted in an increased response in both types of culture and a greater relative effect of PP cells on the evoked PRL release. In contrast to other secretagogues, oxytocin (OT) elicited a smaller response in AP + PP cocultures than in AP cultures. OT was present in significant amounts in medium from cocultures, apparently after being released from the severed neuronal terminals. When AP cultures were pretreated for 4 days with comparable concentrations of OT, the acute OT-evoked PRL release was greatly diminished. These findings suggest that coculture with PP cells increases the releasable pool of PRL in lactotrophs. The stored PRL is accessible for release by secretagogues known to act via the Ca2+ second messenger system, involving both Ca2+/calmodulin and protein kinase-C pathways. The diminished response of cocultures to OT is probably due to desensitization of lactotrophs by the residual amounts of this peptide present in the disrupted nerve endings.
 ...
PMID:Effects of coculture of anterior and posterior pituitary cells on the responsiveness of lactotrophs to different secretagogues. 193 84

Preincubation of Fura 2-loaded rat myometrial cells with H-8, an inhibitor of protein kinase A, for 1 h reversed the inhibitory effects of 8-(4-chlorophenylthio)-cAMP (CPTcAMP) on the oxytocin-stimulated increase in (Ca2+)i (intracellular free calcium), with an EC50 of 47 microM. H-8 also prevented the inhibition by relaxin and isoproterenol of the oxytocin-induced increase in (Ca2+)i. The EC50 of H-8 in reversing the relaxin effect was 42 microM. H-8 reversal of the effect of relaxin on (Ca2+)i was evident both in the absence of extracellular calcium and in cells pretreated with pertussis toxin. H-8 also reversed the inhibitory effects of relaxin and CPTcAMP on the oxytocin-induced increase in [3H]inositol phosphate formation and [3H]phosphoinositide hydrolysis. Preincubation of myometrial cells for 1 h with H-7, another protein kinase inhibitor, only partially attenuated the inhibition by relaxin and CPTcAMP of the oxytocin-induced increase in (Ca2+)i and [3H]inositol phosphate formation at concentrations 4-5 times greater than those of H-8. Acute (15-min) exposure to phorbol myristate acetate (1.0 microM) did not affect basal (Ca2+)i or the oxytocin-stimulated increases in (Ca2+)i or inositol phosphate formation. These results imply a regulatory role for protein kinase A in the inhibition of the oxytocin-induced increase in (Ca2+)i and inositol phosphate formation by relaxants.
 ...
PMID:Involvement of protein kinase A in the regulation of intracellular free calcium and phosphoinositide turnover in rat myometrium. 196 19

Progesterone and estradiol interact to regulate secretion of prostaglandin (PG) F2 alpha from the ovine endometrium in response to oxytocin. Two experiments were conducted to determine if these effects were due to changes in activity of phospholipase C or in the second messenger responsive pathways that regulate production of PGF2 alpha. In both experiments, ovariectomized ewes were assigned to one of four treatment groups (control, estradiol, progesterone, progesterone and estradiol). Steroids were administered, in vivo, to mimic the changes that occur during the estrous cycle. On Day 16 of steroid treatment, endometrial tissue was collected and incubated, in vitro, to measure activity of phospholipase C and release of PGF2 alpha. Treatment with progesterone, in vivo, enhanced basal and oxytocin-induced activity of phospholipase C and release of PGF2 alpha, in vitro. Estradiol suppressed oxytocin-induced activity of phospholipase C, both in the presence and absence of progesterone. In contrast to its effects on phospholipase C, estradiol inhibited basal and oxytocin-induced release of PGF2 alpha when administered alone, but not when administered with progesterone. Steroids had similar effects on the release of PGF2 alpha induced by phorbol 12-myristate 13-acetate and A23187. It was concluded that progesterone and estradiol regulate endometrial release of PGF2 alpha by affecting both the activity of phospholipase C and its associated second messenger responsive pathways that may regulate production of PGF2 alpha.
 ...
PMID:Activity of phospholipase C and release of prostaglandin F2 alpha by endometrial tissue from ovariectomized ewes receiving progesterone and estradiol. 201 59

Incubation of isolated rat adipocytes with insulin, vasopressin, or oxytocin increased plasma membrane-bound protein kinase C (PKC) activity by 100-400%. PKC activity was assayed by a procedure that is virtually background-free, thus permitting assay of protein kinase activity in highly diluted samples of solubilized membranes. Hormone-dependent increases in PKC activity were limited to plasma membranes. Stimulation of the kinase was half-maximal with 70 pM insulin, and the hormone effect was rapid. Oxytocin and vasopressin produced effects on PKC similar to insulin, but the magnitude of the vasopressin stimulation exhibited seasonal variations. Treatment of cells with phorbol 12-myristate 13-acetate (PMA) resulted in a loss of PKC activity from the cytosol and a gain in plasma membrane activity, indicative of translocation of the enzyme. With activity measurements it was not possible to determine if insulin stimulated a translocation of the kinase. However, Western blot analysis of plasma membranes with polyclonal antibodies directed against PKC suggest that at least some of the insulin-stimulated PKC activity resulted from enzyme translocation.
 ...
PMID:Insulin, oxytocin, and vasopressin stimulate protein kinase C activity in adipocyte plasma membranes. 210 94

We investigated effects of various agents on proliferation, intracellular pH (pHi), and intracellular calcium [( Ca2+]i) of rat mesangial cells (MCs) in early passages (2-5). Serum-starved MCs incubated in HCO3- were exposed to one of the following: fetal calf serum (FCS), serotonin, angiotensin II (ANG II), arginine vasopressin (AVP), bombesin (Bom), bradykinin (BK), epidermal growth factor (EGF), epinephrine (Epi), interleukin 1 (IL-1), norepinephrine (NE), neuropeptide Y, oxytocin, substance P (SP), platelet-derived growth factor, or 12-O-tetradecanoylphorbol-13-acetate (TPA). We assessed DNA synthesis from [3H]thymidine uptake during exposure to test agent. All agents except ANG II, NE, Bom, and SP were mitogenic. When MCs were incubated in a HCO3(-) -free N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered medium, maximal mitogenic responses to FCS, AVP, and EGF were 41, 44, and 55% (P less than 0.01) lower, respectively, than those in presence of HCO3-. In absence of HCO3-, agents other than BK and IL-1 produced a biphasic pHi response characterized by a transient acidification followed by a prolonged alkalinization that was both Na(+)-dependent and amiloride-sensitive. In presence of HCO3-, agents produced only a small and gradual acidification, except for IL-1 and Epi. Addition of all agonists except IL-1, EGF, and TPA produced significant transient increases in [Ca2+]i, the magnitudes of which were similar in HCO3- and non-HCO3- buffers. These results demonstrate that, in presence of HCO3-, agents (i.e., NE and ANG II) can produce typical [Ca2+]i transients and still not cause MC proliferation. Conversely, an agent may cause proliferation without eliciting a short-term change in either [Ca2+]i or pHi (i.e., IL-1), a change in [Ca2+]i but not pHi (i.e., Epi), or a change in pHi but not [Ca2+]i (i.e., TPA). Thus, at least for MCs, proliferation in HCO3- can be dissociated from early agonist-induced changes in pHi and [Ca2+]i.
 ...
PMID:Effects of mitogens and other agents on rat mesangial cell proliferation, pH, and Ca2+. 211 98


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>