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Biomedical subjects

A Miyamoto

Publications and source records attributed to A Miyamoto.

At least 163 records · Page 9Linked to original sources
PubMed1996

Roles of dopamine D1 receptors in delta 9-tetrahydrocannabinol-induced expression of Fos protein in the rat brain.

We examined whether administration of delta 9-tetrahydrocannabinol (THC) induces the expression of Fos protein or not in the rat brain. A single administration of 3.2 and 10 mg/kg THC produced a dose-dependent and significant increase in Fos-immunoreactive cells in the striatum, particularly in its dorsomedial portions. The peak increase was reached 2 h after THC treatment and was absent at 8 h. Fos induction was also observed in the nucleus accumbens after administration of 10 mg/kg THC. However, in the globus pallidus, hippocampus and substantia nigra pars reticula, abundant in cannabinoid receptors, there were few or no Fos-immunoreactive cells induced by 10 mg/kg THC. SCH-23390, a selective dopamine D1 receptor antagonist, at 0.32 mg/kg produced a significant block of the effects of THC on Fos expression in the striatum and the nucleus accumbens. Administration of 100 mg/kg (-)-sulpiride, a selective dopamine D2 receptor antagonist, failed to block the effect of THC on Fos expression in both the striatum and the nucleus accumbens. These findings indicate that THC induces the expression of Fos protein and that this expression is mediated at least by dopamine D1 receptors.

Animals↗
PubMed1996

The vasomotor effects of 5-hydroxytryptamine on equine basilar arteries in vitro.

The vasomotor effects of 5-hydroxytryptamine (5-HT) on isolated equine basilar arteries were studied. 5-HT induced contractions of equine basilar arteries in a concentration-dependent manner, with a pEC50 value (with 95% confidence limits) of 7.35 (7.08-7.62). Similar results were obtained with endothelium-denuded basilar arteries. Contractions were not competitively inhibited by the 5-HT2 receptor antagonist ketanserin at low concentrations of 5-HT. Conversely, at high concentrations of 5-HT, contractions were inhibited by ketanserin in a concentration-dependent manner, with a pA2 value of 8.91 (8.62-9.20). The 5-HT1 and 5-HT2 receptor antagonist methiothepin shifted the concentration-response curve of 5-HT downwards and to the right in a concentration-dependent manner. In the presence of 10(-6) mol/L ketanserin, however, methiothepin antagonized 5-HT-induced contractions competitively with a pA2 value of 7.95 (7.59-8.31). The 5-HT3 receptor antagonist MDL 72222 had no effect on 5-HT-induced contractions. The findings of this study indicate that 5-HT1 and 5-HT2 receptors are located in equine basilar arterial smooth muscle cells, and that stimulation of these receptors results in contraction.

Animals↗
PubMed1996

Developmental changes in the noradrenergic innervations of spinal motoneurons in neonatal rats.

Developmental changes in the noradrenergic innervations of spinal motoneurons in both the cervical and lumbar cords were studied in neonatal rats. The labeling of motoneurons was done using choleratoxin B subunit as a retrograde neurotracer. The noradrenergic fibers were detected by immunohistochemistry for tyrosine hydroxylase. At postnatal day 1, tyrosine hydroxylase immunoreactive fibers were evident in the entire ventral horn, including the triceps brachii motoneuron pools at the cervical level. In contrast, they were observed only in that portion of the ventral horn medial to the quadriceps femoris motoneuron pools at the lumbar level. Subsequently, tyrosine hydroxylase immunoreactive fibers increased at both levels, and they were distributed in most of the gray matter at postnatal day 14. At this age, the distribution pattern of tyrosine hydroxylase immunoreactive fibers in the lumbar level was almost identical to that of the cervical level. The number of closely apposed tyrosine hydroxylase immunoreactive varicosities on motoneurons (close appositions) increased continuously from postnatal day 1 to 14 at both the cervical and lumbar levels. At postnatal day 1, triceps brachii motoneurons had more close appositions than quadriceps femoris motoneurons in number and, after postnatal day 7, there was no difference in the number of close appositions between triceps brachii motoneurons and quadriceps femoris motoneurons. Based on these results, we discuss the significance of monoaminergic influences on the postnatal development of spinal motoneurons and of motor behavior with a rostrocaudal gradient.

Adrenergic Fibers↗
PubMed1996

Role of altered beta-adrenoceptor signal transduction in the pathogenesis of cirrhotic cardiomyopathy in rats.

BACKGROUND & AIMS: Attenuated ventricular contractility has been documented in cirrhosis, but the pathogenesis remains unclear. The beta-adrenergic receptor system is critical in modulating cardiac contraction. Therefore, the aim of this study was to clarify beta-adrenoceptor signaling function in a rat model of cirrhosis. METHODS: Cirrhosis was induced by bile duct ligation, whereas controls underwent a sham operation. Myocardial contractility was studied by measuring isolated left ventricular papillary muscle contraction under isoproterenol stimulation. Beta-Adrenoceptor signaling was evaluated by measuring adenosine 3',5'-cyclic monophosphate generation after stimulation with isoproterenol, sodium fluoride, and forskolin. Guanosine triphosphate-binding protein expression from ventricular plasma membranes was determined by Western blots to measure G(s)alpha, Gi2alpha, and G(common)beta, respectively. RESULTS: Maximum papillary muscle contractile responses in control and cirrhotic rats were 113% +/- 3% and 70% +/- 2% of basal, respectively (P<0.01), with no significant differences in the dose-inducing half-maximal response. Adenosine 3', 5'-cyclic monophosphate generation after stimulation with all three agents was significantly lower in cirrhotic compared with control rat membranes. G(s)alpha and Gi2alpha expression was significantly reduced in cirrhotics compared with controls, but G(common)beta expression remained unchanged. CONCLUSIONS: These data showed cardiac contractile impairment in cirrhosis, associated with altered beta-adrenergic receptor signaling function and guanine nucleotide-binding protein expression. These factors may play an important role in the pathogenesis of cirrhotic cardiomyopathy.

Adrenergic beta-Agonists↗
PubMed1996

Effects of local growth factors on the secretory function of bovine corpus luteum during the oestrous cycle and pregnancy in vitro.

The impact of insulin-like growth factor-I (IGF-I) basic fibroblast growth factor (bFGF), endothelin-1 (ET-1), tumour necrosis factor-alpha (TNF-alpha), transforming growth factor-alpha (TGF-alpha) and platelet-derived growth factor (PDGF) on the release of progesterone (P4) and oxytocin (OT) from individual bovine corpora lutea at different stages of the oestrous cycle and pregnancy was evaluated with a microdialysis system (MDS) in vitro. IGF-I (1 microgram mL-1) induced significantly the acute effects on P4 release at the late luteal stage (Days 15-18) and early pregnancy (Days 60-120), whereas bFGF (100 ng mL-1) was extremely effective in stimulating P4 release particularly during the mid-luteal stage (Days 8-12). Both peptides stimulated (P < 0.05) the release of OT throughout the three luteal stages and during early and late pregnancy (Days 30-60 and Days 150-210). ET-1 (100 ng mL-1) clearly inhibited P4 release during the early (Days 5-7) and mid-luteal phase and stimulated OT release only during the mid-luteal stage (P < 0.001). TNF-alpha (100 ng mL-1) stimulated the release of P4 exclusively at the early luteal phase (P < 0.05), whereas OT secretion was increased by TNF-alpha during all stages of the oestrous cycle (P < 0.001). TGF-alpha and PDGF (100 ng mL-1) were effective in stimulating P4 release particularly during late pregnancy (P < 0.05). In contrast, stimulation of OT secretion by TGF-alpha was maximal during the late-luteal stage (P < 0.001), whereas PDGF significantly increased OT secretion during the oestrous cycle (except the early luteal stage) and pregnancy (P < 0.001). The data demonstrate distinct and stage-specific effects of growth factors on P4 and OT secretion in vitro. IGF-I, bFGF and TGF-alpha may play an important role in corpus luteum (CL) function during the oestrous cycle and pregnancy since they are locally expressed and synthesized, there are receptors for these growth factors, and they have been demonstrated to exert biological effects on the CL.

Animals↗
PubMed1996

Assessment of visuoperceptual disturbance in children with spastic diplegia using measurements of the lateral ventricles on cerebral MRI.

The authors estimated perceptual disturbance in children with spastic diplegia from the difference between the visual and performance IQ scores (VIQ-PIQ) on the Wechsler Intelligence Scale for Children-Revised (WISC-R), having found a strong negative correlation between this score and the PQ obtained on the Frostig Developmental Test of Visual Perception (DTVP). The ratio of the areas of the posterior horns to the anterior horns (P/A) correlated negatively with visuoperceptual disturbance. This ratio can therefore be used to assess perceptual disturbance at an early age in children with spastic diplegia.

Adolescent↗
PubMed1996

Helix-loop-helix proteins LYL1 and E2a form heterodimeric complexes with distinctive DNA-binding properties in hematolymphoid cells.

LYL1 is a basic helix-loop-helix (HLH) protein that was originally discovered because of its translocation into the beta T-cell receptor locus in an acute lymphoblastic leukemia. LYL1 is expressed in many hematolymphoid cells, with the notable exceptions of thymocytes and T cells. Using the yeast two-hybrid system to screen a cDNA library constructed from B cells, we identified the E-box-binding proteins E12 and E47 as potential lymphoid dimerization partners for LYL1. The interaction of LYL1 with E2a proteins was further characterized in vitro and shown to require the HLH motifs of both proteins. Immunoprecipitation analyses showed that in T-ALL and other cell lines, endogenous LYL1 exists in a complex with E2a proteins. A preferred DNA-binding sequence, 5'-AACAGATG(T/g)T-3', for the LYL1-E2a heterodimer was determined by PCR-assisted site selection. Endogenous protein complexes containing both LYL1 and E2a bound this sequence in various LYL1-expressing cell lines and could distinguish between the LYL1 consensus and muE2 sites. These data demonstrate that E2a proteins serve as dimerization partners for the basic HLH protein LYL1 to form complexes with distinctive DNA-binding properties and support the hypothesis that the leukemic properties of the LYL1 and TAL subfamily of HLH proteins could be mediated by recognition of a common set of target genes as heterodimeric complexes with class I HLH proteins.

Animals↗
PubMed1996

Role of L-type calcium channels on halothane-induced myocardial depression in cultured rat ventricular myocytes.

The effects of antagonists for L-type Ca2+ channel, opener and blocker to ATP-sensitive K+ (KATP) channel, phosphodiesterase inhibitor, or Ca2+ sensitizer on halothane-induced myocardial depression were investigated in cultured rat ventricular myocytes. Halothane (1 to 4%) decreased the beating rate and amplitude in a dose-dependent manner. Myocardial depressant effects of halothane were potentiated by the presence of 10 nM nifedipine or verapamil. Neither cromakalim (1 microM), glibenclamide (1 microM), nor pimobendan (10 microM) altered the dose-dependent depressant effects of halothane. The mechanisms involving altered KATP channel, cAMP levels or Ca2+ sensitivity of contractile proteins may not be responsible for myocardial depression during halothane exposure. These results suggest that changes in L-type Ca2+ channel function plays an important role in the volatile anesthetic halothane-induced depression of contractile activity in cultured rat ventricular myocytes.

Anesthetics, Inhalation↗
PubMed1996

Stability of free Mg2+ concentration and increased concentration of free Ca2+ in vascular smooth muscle cells during dietary magnesium deficiency in rat.

Intracellular free calcium and magnesium ion concentrations ([Ca2+]i and [Mg2+]i respectively) were estimated in thoracic aorta smooth muscle strips isolated from magnesium-deficient and control rats using fura-2/AM and mag-fura-2/AM, respectively. Adult male Wistar rats were fed a magnesium-deficient diet (10 mg Mg/kg diet) or a control diet (700 mg Mg/kg diet) for 30 days. Plasma magnesium level in magnesium-deficient rats was half of that in control rats at 30th day. Therefore, thoracic aorta strips, denuded of endothelium, were loaded with fura-2/AM or mag-fura-2/AM in the presence of 0.5 or 1.0 mM Mg2+, and [Ca2+]i or [Mg2+]i was measured under the same Mg2+ conditions. The [Ca2+]i in the aorta strips isolated from magnesium-deficient rats in the presence of 0.5 mM Mg2+ (254.9 +/- 13.1 nM) was approximately three times greater than in those from control rats in the presence of 1.0 mM Mg2+ (86.5 +/- 9.2 nM). The [Mg2+]i was not significantly different between the two groups at either Mg2+ level. The muscle tension and [Ca2+]i increased after [Mg2+]o was exchanged from 1.0 to 0.5 mM; however, [Mg2+]i showed no change. The total calcium content increased and total magnesium content decreased in thoracic aorta strips isolated from magnesium-deficient rats. These results suggest that [Mg2+]i is stable, but that [Ca2+]i increases in vascular smooth muscle cells of thoracic aortas isolated from dietary magnesium-deficient rats.

Animals↗
PubMed1995

Effect of repeated administration of delta 9-tetrahydrocannabinol on delayed matching-to-sample performance in rats.

In the present study we examined the effect of repeated exposure to delta 9-tetrahydrocannabinol (THC) at a dose of 10 mg/kg (once a day for 4 days) 24 h after administration, on delayed matching-to-sample (DMTS) performance in rats using a three-lever operant apparatus. Although DMTS performance was not changed on the 1st day, it was impaired on the 2nd day. The impairment was potentiated in dependence of repeated administration. After withdrawal of THC, the impairment of DMTS performance gradually disappeared. On the 10th day after withdrawal, readministration of 10 mg/kg THC resulted in marked impairment of DMTS performance at 24 h after administration. Furthermore, a single administration of 1.0 mg/kg THC 30 min prior to the session, the dose at which a single administration did not cause impairment of DMTS performance in vehicle-treated rats, significantly decreased the number of reinforcements in the test trial. In conclusion, the present study demonstrated that repeated THC administration impaired DMTS performance under the condition of 24 h after administration, and that behavioral sensitization to this impairment developed. Furthermore, the suppressive state of lever-pressing induced by repeated THC administration may be a useful animal model for amotivational syndrome in humans.

Animals↗
PubMed1995

[The significance of platelet alpha 2-adrenoceptor and sympathetic nerve activity in the hypertensive mechanism under essential hypertension--with special reference to pressor response to norepinephrine].

Although many studies have examined the metabolism of catecholamines and cardiovascular responsiveness to norepinephrine in essential and various experimental hypertension, the role of sympathetic nervous system in the pathogenesis of hypertension has not been elucidated. In this study, therefore,the role of sympathetic nerve activity related to platelet alpha 2-adrenoceptor was investigated to clarify the mechanism in which sympathetic nervous system augments the blood pressure elevation in patients with essential hypertension (EHT). Tritiated yohimbine binding was used to estimate platelet membrane alpha 2-adrenoceptor characteristics in 27 hospitalized patients with mild to moderate EHT and 27 normotensive subjects (NT) receiving a regular diet containing 120mEq/day of sodium and 75mEq/day of potassium. In this study, mean arterial pressure (MAP) and plasma norepinephrine concentration (pNE) was significantly higher in EHT than those in NT. Total binding sites (Bmax) and dissociation constant (Kd) for 3H-yoshimbine in EHT was also significantly higher than those in NT. There was a significant positive correlation between Bmax and age in NT, but not in EHT. A significant positive correlation was observed between the pressor response to infused norepinephrine (NE-R:increments in MAP induced by i.v. infused 0.2 micrograms/kg/min of NE) and Bmax both in NT and EHT. On the other hand, no significant correlation was found between NE-R and Kd in NT and EHT. In addition, Bmax was correlated inversely with PNE in both NT and EHT. These findings suggest that down-regulation mechanism exists in platelet alpha 2-adrenoceptor number responded to PNE levels. Moreover, the increased density of alpha-adrenoceptor might have something to do with the augmented NE-R in EHT, indicating an important pathophysiological role of this receptor in the hypertensive mechanisms in EHT.

Adult↗
PubMed1995

Triggering of plaque disruption and arterial thrombosis in an atherosclerotic rabbit model.

BACKGROUND: It is now recognized that plaque disruption and thrombosis, a process often triggered by activities of the patient, is generally the cause of the onset of acute coronary syndromes. Understanding of disease onset could be greatly enhanced by the availability of a suitable animal model of plaque disruption and thrombosis. The aim of this study was to replicate and further characterize an atherosclerotic rabbit model of triggering of arterial thrombosis that was introduced by Constantinides and Chakravarti more than 30 years ago but not subsequently used. Aortic plaques were induced by a high-cholesterol diet, by mechanical balloon injury of the artery, or by a combination of the two. Triggering was attempted by injection of Russell's viper venom (RVV), which is a proteolytic procoagulant, and histamine. METHODS AND RESULTS: A total of 53 New Zealand White rabbits were exposed to one of four preparatory regimens: rabbits in group I (n = 9) were fed a regular diet for 8 months; rabbits in group II (n = 13) were fed a diet of 1% cholesterol for 2 months alternated with 2 months of a regular diet for a total of 8 months; rabbits in group III (n = 5) underwent balloon-induced arterial wall injury, then were given a regular diet for 8 months; and rabbits in group IV (n = 14) underwent balloon-induced arterial wall injury, then were given a diet of 1% cholesterol for 2 months followed by a regular diet for 2 months for a total of 4 months. After completion of the preparatory regimen, triggering of plaque disruption and thrombosis was attempted by injection of RVV (0.15 mg/kg IP) and histamine (0.02 mg/kg IV). In group I, normal control rabbits without atherosclerosis, only one small thrombus was noted in 1 of 9 rabbits. In group II, cholesterol-fed rabbits, thrombosis occurred in 3 of 13 rabbits. Thrombus occurred in all rabbits in group III (5 of 5) and in 10 of 14 rabbits in group IV. Although the frequency of thrombosis was not significantly different between groups I and II, possibly due to a small sample size, it was significantly different among all four groups (P < .001). Also, the frequency and amount of thrombus formation were significantly different among all four groups (P < .001; P < .0001) but not between groups I and II. Rabbits with atherosclerosis (those in groups II and IV) demonstrated plaque disruption and overlying platelet-rich thrombus formation similar to that observed in patients with acute coronary syndromes. The surface area covered by thrombus was 2 mm2 in group I, 15.3 +/- 19.2 mm2 in group II, 223 +/- 119 mm2 in group III, and 263 +/- 222 mm2 in group IV. Rabbits in groups III and IV had the greatest amount of thrombus, and this amount was significantly greater than in rabbits in groups I and II (P < .001 and P < .03, respectively). CONCLUSIONS: A suitable animal model is available for the study of plaque disruption and arterial thrombosis. Hypercholesterolemia and mechanical arterial wall injury seemed to produce plaques vulnerable to triggering of disruption and thrombosis, whereas normal arteries were relatively resistant to triggering. This model provides a method to evaluate agents that might decrease the occurrence of vulnerable plaques or the amount of thrombus formed after triggering. Most important, the model can be used to identify the features of vulnerable plaques and the pharmacological stressors that trigger plaque disruption and thrombus formation.

Animals↗
PubMed1995

Intravascular ultrasound can be used to evaluate pulsed laser ablation of arterial tissue.

BACKGROUND AND OBJECTIVE: Intravascular ultrasound (IVUS) has been used successfully to detect intravascular lesions. This study evaluates the ability of IVUS to detect acoustic damage to the arterial wall following high power, pulsed laser ablation. STUDY DESIGN/MATERIALS AND METHODS: Arterial ablation and disruption were performed in necropsy bovine aorta with a Ho:YAG laser using energy ranging from 140-720 mJ/pulse at 5 Hz. Laser energy was delivered with 2 mm diameter, multifiber over-the-wire catheters. A 20-MHz IVUS catheter was used to image the arterial damage prior to tissue fixation and morphometry. RESULTS: IVUS images revealed ablation craters surrounded by high acoustically backscattering zones. By histology, the arteries revealed ablation craters lined with thermal coagulation surrounded by a region of dissection and vacuolization. The depth and width of the highly backscattering zones on IVUS images correlated strongly with the corresponding morphometric measurements of tissue dissection (r = 0.92, P = 0.0001 and r = 0.80, P = 0.0001, respectively). Morphometric measurements of the ablation crater depth correlated strongly with laser energy (r = 0.90, P = 0.0001), whereas crater width was not correlated with laser energy (r = 0.27, P = 0.09). CONCLUSION: This study demonstrates that IVUS can detect and measure the extent of arterial damage following pulsed laser ablation. This may provide a means of detecting the extent of tissue disruption and help develop approaches to reduce or prevent extensive tissue damage.

Angioplasty↗
PubMed1995

Acute transverse myelitis caused by ECHO virus type 18 infection.

UNLABELLED: A 14-year-old boy developed acute quadriplegia, associated with sensory impairment and bowel and urinary dysfunction. MRI of the cervical cord showed diffuse increased signal intensity on T2-weighted images with gadolinium-diethylenetriamine penta-acetic acid enhancement. Based on the clinical presentation and MRI findings, the diagnosis of acute transverse myelitis was made. Enterovirus RNA was amplified from CSF by the reverse transcriptase-polymerase chain reaction. Serum neutralizing antibody to ECHO virus type 18 rose from 1/4 on admission to 1/16 2 months later. CONCLUSION: This is the first reported case of acute transverse myelitis caused by ECHO virus type 18 infection.

Acute Disease↗
PubMed1995

Alobar holoprosencephaly with diabetes insipidus and neuronal migration disorder.

A 2-year-old girl with alobar holoprosencephaly associated with facial abnormalities, central diabetes insipidus, and a neuronal migration disorder is reported. The diagnosis of diabetes insipidus was based on low urine osmolality and low plasma ADH concentration during a water deprivation test, and clinical and biochemical improvement after desmopressin acetate administration. Because the posterior portion of the pituitary was located in the sella turcica and the hypothalamo-pituitary stalk was intact, the diabetes insipidus was presumed to have been caused by hypothalamic osmoreceptor dysfunction. MRI findings were compatible with alobar holoprosencephaly. In addition, heterotopic gray matter was recognized as a continuous band over a single ventricle. Defective cleavage of the prosencephalon associated with a neuronal migration disorder is characteristic of alobar holoprosencephaly.

Brain↗
PubMed1995

Change of flow cytometric DNA content in para-aortic lymph node showing recurrence after adjuvant chemotherapy for gastric cancer.

A para-aortic lymph node showing recurrence was resected from a patient who had received adjuvant chemotherapy after curative resection of an advanced gastric cancer. A flow cytometric analysis of DNA content was carried out for the primary lesion, a metastatic lymph node and the resected lymph node. A peri-diploid cell population in addition to diploid cells appeared in the recurrent lesion, whereas a major diploid cell population and a minor aneuploid cell population were found in the primary lesion and the metastatic lymph node, indicating that a clone of chemo-resistant tumor cells selectively multiplied after the cytotoxic therapy. The characters of a recurrent lesion may be changed by clonal selection following chemotherapy.

Adenocarcinoma↗
PubMed1995

Effects of prostaglandins and oestradiol-17 beta on oxytocin binding in cultured bovine luteal cells.

The aim of the investigation was to evaluate the possible action of prostaglandins (PGs) and oestradiol-17 beta (oestradiol) on the specific binding for oxytocin in bovine luteal cells. Cultured cells of bovine corpora lutea at the mid-luteal stage (Day 8-12 of the oestrous cycle) were examined for the presence of oxytocin receptors by a radioreceptor assay using the 125I-labelled oxytocin antagonist [d(CH2)5,Tyr(Me)2,Thr4,Tyr-NH29]-vasotocin (125I-OVT) as a ligand. The cells were cultured for 48 h in total. In the final 15 h of culture, the luteal cells were exposed to varying concentrations of PGF2 alpha, PGE2 and/or oestradiol. After culture, the cells were incubated with 37,000 dpm (0.5 nM) 125I-OVT with or without 100 nM of unlabelled oxytocin. PGF2 alpha, at 10(-8) M and 10(-7) M, stimulated the specific binding for oxytocin to levels as high as 128% of controls (P < 0.01); by contrast, PGE2, PGI2 or oestradiol had no effect on oxytocin binding. Scatchard analysis revealed that the concentration of oxytocin receptors was increased (P < 0.05) from 6.7 fmol micrograms-1 DNA to 8.4 fmol micrograms-1 DNA by stimulation with 10(-7) M of PGF2 alpha without changing the binding affinity. No further increase in the specific binding was observed when PGF2 alpha was used in combination with PGE2, PGI2 or oestradiol at a concentration of 10(-7) M. Addition of indomethacin (28 microM) resulted in the inhibition of PGF2 alpha secretion, coinciding with a significant decrease in oxytocin binding (P < 0.01). However, addition of arachidonic acid (100 microM) caused a significant increase in the secretion of PGF2 alpha and the specific binding for oxytocin concomitantly (P < 0.05). When the protein kinase C (PKC) activity of the luteal cells was inactivated by preincubating cells for 13 h with 1 microM phorbol 12-myristate 13-acetate before PGF2 alpha stimulation, the specific binding for oxytocin was not affected by PGF2 alpha stimulation (10(-7) M) in the final 15 h of culture. These data suggest that PGF2 alpha may be one of the potent regulators for luteal oxytocin receptors in a paracrine and/or autocrine manner, and that its action is mediated by PKC.

Animals↗