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1.
T-2 toxemia and brain prostaglandins 总被引:1,自引:0,他引:1
T-2 toxin is a trichothecene mycotoxin which is a member of a family of closely related sesquiterpenoids. It was recently shown that T-2 toxemia is associated with elevated plasma levels of eicosanoids. To study further the effect of T-2 on the cyclooxygenase pathway of arachidonate we examined the release of PGE2, TXB2 and 6-keto-FGF1 alpha from brain tissue exposed to T-2 toxin in vivo or in vitro. Administration of T-2 toxin (0.75 or 2 mg/kg) to conscious rats caused a transient increase in the rate of the release of 6-keto-PGF1 alpha and TXB2 from brain slices taken from the cortex (C); no effect was found in the hypothalamus (HT) or the nucleus tractus solitarius (NTS) region of the medulla oblogata. PGE2 showed time and dose related increments (over 5 folds) in both the C and HT but not in the NTS. Incubation of cortical or hypothalamic slices in oxygenated Krebs buffer with a wide range of T-2 toxin concentrations (10(-9)-10(-3) M) demonstrated a complex response: stimulation of PGE2 and TXB2 release from C slices at 10(-7) M (greater than 40%, p less than 0.01 and 20%, p less than 0.05, respectively) and inhibition at high concentrations (greater than 10(-4) M) of all PGs studied. Hypothalamic slices showed decrease in all PGs released by very low (10(-9)-10(-8)) or very high (10(-4) M) concentrations of T-2. These studies are consistent with the possibility that the arachidonate cascade in the central nervous system might have a role in the pathophysiology of trichothecene mycotoxicosis. 相似文献
2.
Ronald H. Goldstein Margaret Wall Linda Taylor Michael Cahill Peter Polgar 《Prostaglandins & other lipid mediators》1984,28(5):717-729
Pretreatment of human lung fibroblasts with PGE2 but not PGF2α enhanced synthesis of prostaglandins (PGs). The effect of the pretreatment on PG synthesis was related to the concentration of PGE2 that was added to the culture medium. Pretreatment with PGE2 at 5 × 10−12M did not enhance PG synthesis whereas pretreatment with PGE2 at 5 × 10−6M induced a maximal effect. Production of PGs was increased following 1 day of pretreatment with PGE2 and was increased further following 3 days of pretreatment. The PGE2 treated cells showed only a slight increase in the bradykinin-induced release of radioactivity from cells prelabeled with [3H]arachidonic acid but showed a dramatic increase in the bradykinin-induced synthesis of radio-labeled PGs. The conversion of free arachidonate to PGs in both intact cells and in a cell-free preparation was increased by PGE2 pretreatment. The presence of cyclohexamide during the pretreatment did not inhibit the PGE2-induced activation of PG synthesis. Taken together, the results indicate that pretreatment of cells with PGE2 increased PG synthesis by augmenting the conversion of arachidonate to PGs. 相似文献
3.
Prostaglandins (PGs) E1 or F1α (1.4−8.4 × 10−8 M) contracted strips of rabbit aorta and increased the contractions produced by 1−6 × 10−7 M phenylephrine (PE). The addition of the PGs simultaneously with PE or after a low concentration of PE (2 × 10−7 M) significantly increased the PE-induced contractions. However, when the PGs were added after a higher concentration of PE (6 × 10−7 M) an additional increase in the PE-induced contraction was produced with PGF1α but not with PGE1. Isobolic plots of the data obtained from the simultaneous addition of PE and the PGs indicate that both PGs interact with PE in a synergistic or potentiative manner, suggesting that their effects are mediated through different receptor mechanisms. Addition of the PGs after a high dose of PE indicates that there may also be either qualitative or quantitative differences between PGE1 and PGF1α. 相似文献
4.
Role of prostaglandins in calcium-induced corticosteroid secretion by isolated frog interrenal gland
I. Lihrmann C. Delarue F. Homo-Delarche P. Netchitailo F. Leboulenger H. Vaudry 《Prostaglandins & other lipid mediators》1986,32(1):127-131
The role of prostaglandins (PGs) in calcium-induced corticosteroid secretion by frog adrenal (interrenal) gland examined
using a perifusion technique. Increasing concentrations of CaCl2 (4–10 mM) stimulated in a dose-dependent manner aldosterone, PGE2 and 6-keto-PGF1α production, whereas TXB2 was not affected. The kinetics of the adrenal response to CaCl2 indicated that the increase in PG output always preceded that of steroid. Administration of cobalt (4 mM), a calcium-channel inhibitor, blocked the calcium-induced stimulation of PGs and corticosteroids. Infusion of indomethacin (5 × 10−6M), a specific cyclooxygenase inhibitor, significantly decreased the basal production of PGs and steroids, and prevented the stimulatory effect of CaCl2 (6 mM). Infusion of the calcium ionophore A 23187 (10−6 M), for 20 min, induced a marked stimulation of PG and steroid production. Taken together, these data support the notion that biosynthesis of prostaglandins is associated with calcium-induced corticosteroid secretion in frog adrenal cells. 相似文献
5.
M. Viggiano A.M. Franchi A. Faletti M.A.F. Gimeno A.L. Gimeno 《Prostaglandins & other lipid mediators》1988,36(3)
The effects of exogenous histamine (H) on prostaglandin (PG) generation and release in uteri isolated from diestrous rats and the influences of H2-receptors blockers (cimetidine and mitiamide) on the output of uterine PGs, were explored. Moreover, the action of H on the uterine 9-keto-reductase, was also studied. Histamine (10−4M) failed to alter the basal output of PGE1 but reduced significantly the generation and release of PGE2 and augmented the output of PGF2α. On the other hand, cimetidine (10−5M) enhanced the basal release of PGE2 but had no action on the outputs of PGs E1 or F2α. The enhancing effect of H on the production and release of PGF2α was abolished in the presence of cimetidine. Also, the antagonist reversed the influence of H on the output of PGE2. Metiamide, another H2-receptor antagonist, did not alter the basal control generation and release of uterine PGs, but antagonized the augmenting influence of H on PGF2α uterine output, as much as cimetidine did, and prevented the depressive action of H on the release of PGE2 from uteri. Histamine (10−4M) significantly stimulated uterine formation of cyclic-adenosine monophosphate, an action which was antagonized by the presence of cimetidine (10−5M), a blocker of H2 receptors. Also, histamine (10−5M) and dibutyril-cyclic-adenosine monophosphate (DB-cAMP) at 10−3M, enhanced significantly the formation 3H-PGF2α from 3H-PGE2. Results presented herein demonstrate that H is able to diminish the generation of PGE2 in uteri from rats at diestrus augmenting the synthesis of PGF2α, apparently via the activation of H2-receptors, enhancing adenylate-cyclase. These effects appear to increase uterine 9-keto-reductase activity which transforms PGE2 into PGF2α. Relationships between the foregoing results and those evoked by estradiol, are also discussed. 相似文献
6.
Specificity of the effect of prostaglandins (PGs) on hormone release by the anterior pituitary gland was studied using cells in primary culture. Growth hormone (GH) release is stimulated by all eight PGs studied, PGE1 and E2 being 1000-fold more potent than the corresponding PGFs. The release of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and prolactin (PRL) remains unchanged upon addition of PGEs. While the basal release of thyrotropin (TSH) is only slightly stimulated by concentrations of PGEs above 10−6M, an important potentiation of the stimulatory effect of thyrotropin-releasing hormone on TSH release is observed. The release of GH, TSH and LH is stimulated equally well by PGAs and PGBs at concentrations higher than 10−6M, 3 × 10−6M, and 10−5M, respectively. PGFs do not affect the release of any of the measured pituitary hormones at concentrations below 10−4M. The stimulation of GH release by PGE2 can be inhibited by the PG antagonist 7-oxa-13-prostynoic acid, a half-maximal inhibition being found at a concentration of 4 × 10−5M of the antagonist in the presence of 10−6M PGE2. In the presence of somatostatin (10−8M), the inhibition of GH release cannot be reversed by PGE2 at concentrations up to 10−4M. 8-bromo-cyclic AMP-induced GH release is additive with that produced by PGE2.The present data show that 1) of the five pituitary hormones measured, only GH release is stimulated by prostaglandins at relatively low concentrations, 2) the PGE-induced GH release can be competitively inhibited by 7-oxa-13-prostynoic acid, 3) the inhibition of GH release by somatostatin cannot be reversed by PGE2 and 4) the PGEs increase the responsiveness of the thyrotrophs to TRH. 相似文献
7.
Continuously superfused rat anterior pituitary cells were used to study the effects of exogenous prostaglandins (PGs) and thromboxanes (TXz) on the secretion of prolactin (PRL). No change in hormone release was observed upon superfusion with TXB2 (10−5M) or the TX synthesis inhibitor, imidazole (1.5 mM). PGs A2, B2, d2, e1, e2, f1α, F2α, and endoperoxide analogs, U-44069 and U-46619, also had no effect on PRL secretion (all at 10−5M), In contrast 10−5M PGI2 was repeteadly found to stimulate PRL release to a level at least 125% above control, while producing no apparent change in the amount of hormone secreted in response to TRH. Somatostatin (SRIF), at a dose of 10−M, maximally inhibited TRH-induces PRL output, but failed to alter the PRL response to PGI2. These studies indicate that PGI2 may have a direct effect on the anterior pituitary to modify PRL secretion. 相似文献
8.
The effect of PGE2 on catecholamine release from human adrenal medulla and phaechromocytoma was studied in slices incubated
. In each of 3 normal human adrenal medullae PGE2 (10−7 M) caused a significant inhibition of the release of catecholamines in
incubation. In each of 3 phaeochromocytomas studied PGE2(10−7 M) caused a significant increase of catecholamine release in
incubation. The possible relevance of this mechanism to the regulation of catecholamine release in phaeochromocytoma is discussed. 相似文献
9.
Frank C. Grenier Margaret L. Allen William L. Smith 《Prostaglandins & other lipid mediators》1982,24(4):547-565
To determine the influence of prostaglandins on cAMP metabolism in renal papillary collecting tubule (RPCT) cells, intracellular cAMP levels were measured after incubating cells with prostaglandins (PGs) alone or in combination with arginine vasopressin (AVP). PGE1, PGE2 and PGI2, but not PGD2 or PGF2α, increased intracellular cAMP concentrations. At maximal concentrations (10−5
tthe effects of PGE2 plus PGI2 (or PGE1), but not of PGI2 plus PGE1, were additive suggesting that at least two different PG receptors may be present in RPCT cell populations. Bradykinin treatment of RPCT cells caused an accumulation of intracellular cAMP which was blocked by aspirin and was quantitatively similar to that observed with 10−5
PGE2. PGs, when tested at concentrations (e.g. 10−9
) which had no independent effect on intracellular cAMP levels, did not inhibit the AVP-induced accumulation of intracellular cAMP in RPCT cells. These results indicate that PGs do not block AVP-induced accumulation of intracellular cAMP in RPCT cells at concentrations of PGs which have been shown to inhibit the hydroosmatic effect of AVP on perfused collecting tubule segments. However, at higher concentrations of PGs (e.g. 10−5
), the effects of AVP plus PGE1, PGE2, PGI2 or bradykinin on intracellular cAMP levels were not additive. Thus, under certain conditions, there is an interaction between PGs and AVP at the level of cAMP metabolism in RPCT cells. 相似文献
10.
Effects of prostaglandins (PGs) E1, E2, F2α and I2 in a wide range of concentration were examined in mesenteric and cerebral arteries isolated from mature baboons. PGs E1, E2 and F2α at low concentrations (10−10 to 10−7 M) elicited relaxation in helically cut strips of cerebral arteries precontracted with phenylephrine. In contrast, the PGs did not cause relaxation in the mesentric artery. PGI2 (10−9 to 10−6 M) produced marked relaxation in both arteries. The EC25 for PGI2 in the mesenteric artery was significantly lower than that in the cerebral artery. During baseline conditions, cerebral arteries contracted in response to high concentrations (greater than 10−7 M) of PGs E1, E2 and F2α. In mesentric arteries, a large contraction was induced by PGs F2α and E2 but not by PGE1. Arachidonic acid (10−6 M) produced an aspirin-inhibitable relaxation in both arteries to a similar extent, so that the vasodilator PG(s) formed in the two different arterial walls appear to exert a similar relaxant action. Thus, the baboon mesenteric artery was more sensitive to PGI2 for the relaxant effect than was the cerebral artery, while PGs F2α, E1 and E2 caused only a contraction in the mesenteric artery but both relaxation and contraction in the cerebral artery. 相似文献
11.
A. Faletti M. A. Chaud M. A. F. Gimeno A. L. Gimeno 《Prostaglandins, leukotrienes, and essential fatty acids》1988,34(3)
The effects of morphine on the constancy of spontaneous contractions (isometric developed TENSION = IDT and contractile FREQUENCY = CF), in uterine strips isolated from ovariectomized rats and the influence of naloxone, were explored. The inotropic responses to added prostaglandins (PGs) E2 and F2α and the influences of morphine and of morphine in the presence of naloxone on PG actions, were also determined. Moreover, the synthesis and outputs of PGs E and F from uteri and the effects of morphine alone and of morphine plus naloxone, were studied. Morphine (10−6 M) significantly depressed uterine constancy of IDT during the first hours following delivery, but its action on CF did not differ from controls. Naloxone, neither at 10−8 M nor at 10−6 M, altered the negative inotropoic influence of morphine on IDT. Exogenous PGs E2 and F2α, stimulated uterine inotropism in a concentration-dependent fashion. Morphine altered dose-response curves for exogenous PGE2, evoking a parallel surmountable shift to the right, but did not affect the inotropic action of added PGF2α. This antagonistic effect of the opioid was not altered by preincubation with naloxone. Basal synthesis and outputs of PGs E and F in uteri from ovariectomized rats were significantly depressed by morphine (10−6 M) but not altered by incubating tissues with morphine in presence of naloxone. Results are discussed in terms of a presumptive dual action of morphine on uterine motility, i.e., antagonizing PGE2 receptors and inhibiting the synthesis of some PGs by the uterus. These influences of morphine do not appear to be subserved by the activation of μ opioid receptors. Moreover, the possibility that endogenous opioids could play a relevant role modulating uterine PG influences, is also discussed. 相似文献
12.
M. Hamon J. Berthaut A. Wisner F. Dray B. Descomps H.Thaler Dao 《Prostaglandins & other lipid mediators》1993,46(3)
We studied PGE2 specific binding sites in human myometrial microsomes prepared from uterine specimens obtained by hysterectomy (women between 38 and 55 years of age). Competition experiments showed that the potency order for various prostaglandins (PGs) was : PGE2 ≥ PGE1 PGF2α > Iloprost ≥ Carbacyclin ZK 110841 (PGD2 analogue). These relative affinities indicated that the receptor was of the EP type.In kinetic experiments GTP, GppNHp and GTPγS increased the rate of PGE2 binding (steady state was reached more rapidly in the presence of nucleotides) but maximal specific binding was not significantly different. Complete dissociation could not be obtained, even in the presence of GTP. Only 50% of maximal binding was readily dissociable. The dissociation rate was 4.56.10−4 sec−1 (half time of about 660 sec) and in the presence of GTP analogues it was slightly increased (k−1 = 7.16 10−4 sec−1 half time 420 sec.). Scatchard analysis of saturation curves showed an increase in ligand receptor affinity in the presence of GTP or nucleotide analogues: the Kd shifted from 9.66 ± 2.8.10−9 M to 4.96 ± 1.25.10−9M, but the number of binding sites did not change significantly (310 ± 37 to 350 ± 17 fmol/mgP). The effect of GTP was observed at a concentration of 5.10−4M. GppNHp and GTPγS were effective at 1.10−5M. Pretreatment of myometrial membranes with pertussis or cholera toxins had no effect on PGE2 binding to membrane sites. Our conclusion is that GTP induced conversion of a population of low affinity sites into a population of higher affinity sites. This effect of guanine nucleotides was described in adipocytes and kidney medulla.Competition studies with PGE2 analogues (sulprostone, 17-phenyl-ω-trinor PGE2, M&B 28,767, misoprostol, butaprost) showed that this receptor mediates a contractile response and is probably an EP3 subtype. 相似文献
13.
Patricia A. Craven Frederick R. DeRubertis 《Prostaglandins & other lipid mediators》1983,26(4):583-604
Prostaglandin (PG) synthesis and degradation were examined in different regions (epithelial versus non-epithelial structures) of the rat distal colon by both HPLC analysis of [14C] arachidonate (AA) metabolites and by specific radioimmunoassays. Intact isolated colonic epithelial cells synthesized mainly PGF2α and TXA2, as monitored from the formation of its stable degradation product TXB2 (PGF2α > TXB2 > 6-keto-PGF1α, the stable degradation product of PGI2=PGD2=PGE2=13,14-dihydro-15-keto-PGF2α). The profile of PG products of isolated surface epithelial cells was identical to that of proliferative epithelial cells. However, generation of PGs by surface epithelium was 2 to 3-fold higher than by proliferative cells both basally and in the presence of a maximal stimulating concentration (0.1 mM) of AA. The latter implied a greater synthetic capacity of surface epithelium, rather than differences due to endogenous AA availability. The major sites of PG synthesis in colon clearly resided in submucosal structures; the residual colon devoid of epithelial cells accounted for at least 99% of the total PGs produced by intact distal colon. The profile of AA metabolites formed by submucosal structures also differed markedly from that of the epithelium. The dominant submucosal product was PGE2. PGE2 and its degradation product 13,14-dihydro-15-keto-PGE2 accounted for 63% of the PG products formed by submucosal structures (PGE2 PGD2 > 13,14-dihydro-15-keto-PGE2 > PGF2α=TXB2=6-keto-PGF1α > 13,14-dihydro- 15-keto-PGF2α). By contrast, epithelial cells, and particularly surface epithelium, contributed disproportionately to the PG degradative capacity of colon, as assessed from the metabolism of either PGE2 or PGF2α. When expressed as a percentage, epithelial cells accounted for 71% of total colonic PGE2 degradative capacity but only 23% of total colonic protein. Approximately 15% of [3H] PGE2 added to the serosal side of everted colonic loops crossed to the mucosal side intact. Thus, at least a portion of the PGE2 formed in the submucosa reaches, and thereby can potentially influence functions of the epithelium. 相似文献
14.
Steven L. Kunkel Kip Kaercher Micheal Plewa Joseph C. Fantone Peter A. Ward 《Prostaglandins & other lipid mediators》1982,24(6):789-799
Mononuclear phagocytes are knwon to play a key role in various phlogistic reactions by synthesizing and releasing products that may potentiate or inhibit inflammatory processes. The expression of these products appears to be dependent on the source of the macrophage population as well as the stimulus employed. We have studied superoxide anion (O2−) production as well as the generation of PGE2, PGF2α, and TXB2 from resident, oil-elicited and thiogylcollate-induced peritoneal macrophages in mice in the presence and absence of chemotactic peptides. Production of O2−, occurred only in elicited macrophages stimulated with high concentrations of FMLP or C5a; resident cells stimulated with either of the chemotactic peptides were completely unresponsive. Although resident peritoneal macrophages incubated with chemotactic peptides did not generate O2−, these cells did secrete significant levels of PGE2, PGF2α, and TXB2 in response to C5a. FMLP had no stimulatory effect. Elicited macrophages generated increased levels of PGE2 and PGF2α when incubated with C5a. However, production of TXB2 was not stimulated. FMLP was inactive in stimulating PGE2, PGF2α, and TXB2 in all types of macrophages studied. These studies indicate a heterogeneity in the production of inflammatory mediators from various macrophage populations in response to chemotactic factors. 相似文献
15.
The present study investigated the effect of prostaglandins (PG) on the in vitro production of polyclonal IgG and IgM by pokeweed mitogen- stimulated normal human peripheral mononuclear cells. Concentrations of PGE1 and PGA1 in excess of 10−6M were suppressive. PGE2 and PGs of the F series were less effective and significant suppression was seen in concentrations greater than 10−3M. Indomethacin added to cell cultures did not enhance Ig production. This discrepancy between physiologic PG concentrations and the very large pharmacologic concentration necessary to suppress Ig synthesis in vitro makes the physiologic role of PG in the modulation of Ig synthesis questionable. 相似文献
16.
John F. Gerkens John G. Gerber David G. Shand Robert A. Branch 《Prostaglandins & other lipid mediators》1978,16(5):815-823
Prostaglandins (PG)I2, PGE2 and 6-keto PGF1α were infused directly into the gastric arterial supply at 10−9, 10−8 and 10−7 g/kg/min during an intra-gastric artery pentagastrin infusion in anesthetized dogs. 6-keto PGF1α was also infused at 10−6 g/kg/min. Gastric arterial blood flow was measured continuously with a non-cannulating electromagnetic flow probe and gastric acid collected directly from the stomach. PGI2 and PGE2 produced similar dose-dependent increases in blood flow with an increase of more than four-fold at the highest dose. Both PGs inhibited acid output over this dose range with PGE2 having 10 times the potency of PGI2. 6-keto PGF1α was at least 1000 times less active than PGI2 or PGE2 at increasing blood flow and failed to inhibit acid output even at 10−6 g/kg/min. 相似文献
17.
Y. Hata S. Ota T. Nagata Y. Uehara A. Terano T. Sugimoto 《Prostaglandins & other lipid mediators》1993,45(2)
We have established primary colonic epithelial cell culture from adult rabbits and examined effects of anti-inflammatory drugs on prostaglandin (PG) E2 production. Colonic epithelium of adult rabbits was scraped and minced into small pieces. They were incubated for isolation in Hanks' balanced salt solution with 0.35 % collagenase and Earle's solution with 1 mM EDTA. Isolated cells were cultured in Coon's modified Ham's F-12 medium with 10 % fetal bovine serum and antibiotics on collagen coated cell wells. The medium was refed twice a week. The production of PGs was assessed by high pressure liquid chromatography (HPLC). PGE2 and PGF2α were measured by radioimmunoassay. Within 24 hours after inoculation, the cell clumps attached to the surface of the wells and cells began to spread out and grow. Monolayer cultures became confluent in 4 days. Phase contrast microscopy showed that these cells consisted of a homogeneous population of epithelial cells with large oval nuclei, polyhedral shape, and organized sheet-like growth pattern. HPLC profile showed synthesis of 6-keto-PGF1α, thromboxane B2, PGF2α, PGE2, and PGD2 by cultured cells. Quantitatively, 117±7 ng/mg-protein/hour PGE2 by 7.4±0.7 ng/mg-protein/hour PGF2α were produced. While hydrocortisone (10−4-10−2 M) did not show a significant effect on PGE2 production, indomethacin (10−8-10−6 M), and 5-aminosalicylic acid (2×10−4-5×10−3 M) inhibited PGE2 production. We have established relatively convenient procedure for primary culture of colonic epithelial cells from adult rabbits. Different actions of anti-inflammatory drugs on PGE2 synthesis suggest that these cultured cells might be a good tool for the various cellular functional studies of normal colonic epithelial cells. 相似文献
18.
The effects of prostaglandin E2 (PGE2) and indomethacin on excitatory neuro-effector transmission in the human bronchus were investigated by tension recording and microelectrode methods. PGE2 (10−10–10−9M) suppressed the amplitude of twitch contractions and excitatory junction potentials (e.j.ps) evoked by field stimulation at a steady level of basal tension obtained by the combined application of indomethacin (10−5M) and FPL55712 (10−6M). In doses over 10−8M, PGE2 reduced the muscle tone and dose-dependently suppressed the amplitude of twitch contractions. Indomethacin (10−5 or 5 × 10−5M) reduced the muscle tone and enhanced the amplitude of twitch contractions and e.j.ps evoked by field stimulation in the presence of FPL55712. PGE2 (10−9M) had no effect on the post-junctional response of smooth muscle cells to exogenously applied acetylcholine (ACh) (4 × 10−7M). However, indomethacin (10−5M) significantly enhanced the ACh-induced contraction of the human bronchus. These results indicate that PGE2 in low concentrations has a pre-junctional action to inhibit excitatory neuro-effector transmission in addition to a post-junctional action, presumably by suppressing transmitter release from the vagus nerve terminals in the human bronchial tissues. 相似文献
19.
C. Delarue F. Leboulenger F. Homo-Delarche M. Benyamina I. Lihrmann I. Perroteu H. Vaudry 《Prostaglandins & other lipid mediators》1986,32(1)
The role of prostaglandins (PGs) in the mechanism of action of acetylcholine (ACh) on frog adrenocortical cells has been examined. Administration of a single dose of ACh (5 × 10−5 M) to perifused frog interrenal fragments, for 20 min, stimulated the production of corticosterone, aldosterone, PGE2 and 6-keto-PGF1α. In contrast ACh did not significantly alter TXB2 production. The effect of ACh could be mimicked by muscarine (10−5 M). Conversely, nicotine (10−6 to 10−4 M) was totally inactive. The increase in PG biosynthesis preceded the peak of corticosteroid release. Repeated 20-min pulses of ACh (5 × 10−5 M) or muscarine (10−5 M) given at 130-min intervales induced a desensitization phenomenon. In presence of indomethacin (5 × 10−6 M), the effect of ACh on PG and steroid secretion was totally abolished. In calcium-free medium, the effect of ACh on PG and corticosteroid production was completely blocked. These results indicated that, in the frog, ACh stimulates corticosteroid secretion through a PG-dependent mechanism. 相似文献
20.
Leslie D. Boucher Theodore A. Kotchen Brian A. Jackson 《Prostaglandins & other lipid mediators》1986,31(1):143-155
The aim of this study was to determine whether hyperreninemia in the adrenalectomized (ADX) rat is dependent on renal prostaglandin synthesis, as has been suggested for two other hyperreninemic conditions, Bartter's syndrome and chronic liver disease.Plasma renin concentration (PRC) in anesthetized, ADX rats was significantly increased (Δ +480%; p < 0.001) compared to sham-operated controls.
, indomethacin (10 mg/kg i.v.) significantly reduced PRC of anesthetized, ADX rats after both 45 min (Δ −34%; p < 0.05) and 90 min (Δ −47%; p < 0.05).
renin release from renal cortical slices of ADX rats was also significantly greater (Δ +130%; p < 0.05) than from sham-operated control cortical slices. Renin release from cortical slices of ADX rats given dexamethasone (10 μg/kg/day) for 4 days prior to sacrifice did not differ from sham-operated control values.Prostaglandin E2 (PGE2) release from cortical slices of ADX rats did not differ significantly from controls. However, PGE2 synthesis in glomeruli microdissected from ADX rats was significantly increased (Δ +110%; p < 0.001) compared to controls. PGE2 synthesis in glomeruli of dexamethasone-treated ADX rats remained significantly elevated compared to controls. Ibuprofen (10−6 M) decreased PGE2 synthesis in cortical slices by 80%. However, prostaglandin synthesis inhibition had no effect on renin release from either ADX or control renal cortical slices.These results suggest that despite increased glomerular synthesis, prostaglandins do not directly influence renin release in the ADX rat. 相似文献