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1.
The release of prostacyclin from chopped myometrial fractions of 18–20 day pregnant rats was assayed by inhibition of ADP-induced aggregation of citrated rabbit platelet-rich plasma. Preincubation of myometrial tissue with oxytocin 10 mU/ml increased prostacyclin generation from 2.25 ± 0.48 (control) to 3.75 ± 0.73 ng/mg over 15 minutes. Bradykinin 20 μg/ml also caused a significant increase in myometrial prostacyclin output from 2.26 ± 0.19 to 4.26 ± 0.64 ng/mg. PGF2α 1 μg/ml did not increase prostacyclin release significantly. Pretreatment of myometrial tissue with the phospholipase inhibitor mepacrine significantly reduced the peptide-stimulated release of prostacyclin. The results suggest that prostacyclin production may play an important role in modulating the actions of oxytocin and bradykinin in the pregnant rat myometrium. 相似文献
2.
Arachidonic acid, bradykinin and phospholipase A2 modify both prolactin binding capacity and fluidity of mouse hepatic membranes 总被引:3,自引:0,他引:3
J R Dave R A Knazek S C Liu 《Biochemical and biophysical research communications》1981,103(2):727-738
The objective of this study was to determine if arachidonic acid, a precursor of prostaglandin synthesis, bradykinin, a decapeptide known to stimulate membrane phospholipid methylation, arachidonic acid release and prostacyclin synthesis, and enzyme phospholipase A2, capable of liberating arachidonic acid, alter the fluidity of hepatic membranes which could in turn modify the functionality of prolactin receptors. Liver homogenates of adult C3H female mice incubated at 28°C for various times with 1–20 μg/ml arachidonic acid, 1–100 μg/ml bradykinin or 0.26–0.00026 U/ml phospholipase A2 provided the 100,000 × g membrane pellets for subsequent ovine prolactin binding and membrane fluidity studies. Membrane microviscosity was determined by fluorescence polarization techniques using the lipid probe 1,6 diphenylhexatriene. Arachidonic acid, bradykinin and phospholipase A2 stimulated specific oPRL binding, in a dose-related fashion, with maximum increases of 73%, 21% and 46%, at 4 μg/ml arachidonic acid, 5 μg/ml bradykinin and 0.026 U/ml PLA2, respectively. This induction, occurring within 30 min of incubation, was found to be due to an increase in the number of receptor sites. Under the same conditions, arachidonic acid, bradykinin and PLA2 induced 22%, 16%, and 18% decreases in membrane microviscosity, respectively. These data suggest that prostaglandin synthesis modifying agents may modulate the number of prolactin receptors by changing the lipid fluidity of the target cell membranes by either of their known effects: arachidonic acid release from the phospholipid matrix, synthesizing appropriate prostaglandins at correct concentration or methylation of membrane phospholipids. 相似文献
3.
J. Bult E. Wechsung A. Houvenaghel A.G. Herman 《Prostaglandins & other lipid mediators》1981,21(6):1045-1058
Aggregation of chicken thrombocytes was studied in whole blood using an electronic aggregometer. Serotonin (5-hydroxytryptamine, 5HT), arachidonic acid (AA) and collagen, but not adenosinediphosphate (ADP) induced aggregation. Prostaglandin (PG) endoperoxides were essential for arachidonic acid-induced aggregation, but were not involved in 5HT-induced aggregation, as indicated by inhibitory studies with indomethacin. Similar experiments indicated that biosynthesis of endogenous PG endoperoxides contributed to the aggregation induced by low concentrations of collagen, but was of little importance when high collagen doses were employed. PGE1 and PGE2 could abolish all types of aggregation studied, whereas prostacyclin (PGI2) and PGD2 were without any anti-aggregatory activity at 1 μg/ml. Between 1 and 100 ng/ml PGE1 and PGE2 inhibited arachidonic acid- and 5HT-induced aggregation dose-dependently.The lack of any hemostatic function of PGI2 in chickens was also indicated by the absence of biosynthesis of endogenous PGI2 in chicken aorta. PGI2 was assessed as anti-aggregating activity, released by aortic fragments stirred in rabbit platelet rich plasma. Still, the presence of chicken aortic tissue i chicken whole blood inhibited 5HT-, but not arachidonic acid-induced aggregation. This inhibition was not affected by pretreatment of the aortic fragments with indomethacin or pargyline. 相似文献
4.
Vimla Band Rajive Kumar S.M. Kharbanda A.H. Band K. Murugesan A. Farooq 《Prostaglandins & other lipid mediators》1985,30(2):323-333
A sensitive platelet aggregation-inhibition assay was used to quantitate the production of prostacyclin by different cell types of the goat ovary. The assay could detect as low as 0.16 ng in the test sample. Different cell types i.e. granulosa, theca and corpus luteum or the total ovarian homogenate were incubated at 37° C for 10 minutes with or without 0.2mM arachidonic acid. Rat aortic strips were incubated under similar conditions as a positive control. Under basal conditions the amount of prostacyclin produced by corpus luteum cells was higher compared to that by granulosa cells. When the precursor of prostaglandins (arachidonic acid) was provided the production markedly increased in corpus luteum, granulosa, and ovarian homogenate as well as in aortic strips. Theca cells did not produce detectable levels of prostacyclin even when the precursor was provided. Trapidil did not alter the basal but enhanced the archidonic acid-stimulated prostacyclin production in homogenate and granulosa cells with no further increase in corpus luteum cells. U-51605 decreased basal as well as arachidonic acid-stimulated prostacyclin production in all the cell types. The prostacyclin production in ovaries is compartmentalized suggesting a possible role in ovarian physiology. 相似文献
5.
R.D. Nolan G.J. Dusting J. Jakubowski T.J. Martin 《Prostaglandins & other lipid mediators》1982,24(6):887-902
Cyclo-oxygenase products of arachidonic acid metabolism formed by the pericardium and epicardial surface of dog heart were identified and quantitated by radioimmunoassay after separation by high-pressure liquid chromatography. Pieces of pariental pericardium, of dog, ox and rat, when incubated
produced mainly 6-keto-PGF1α, with lesser amounts of PGE2, PGF2α and thromboxane B2. Biosynthesis of all prostanoids increased during incubation of the pariental pericardium of each species with arachidonic acid, but 6-keto-PGF1α was still the major metabolite. When slices of dog heart were incubated with arachidonic acid (1 μg/ml) the rates of 6-keto-PGF1α formation by the pariental pericardium was much greater than that of the myocardium and endocardium. Epicardial slices appeared to be intermediate in 6-keto-PGF1α formation. The hearts of anesthetized dogs were also irrigated
with Krebs' solution, and during the first 5 min of epicardial irrigation the pericardial fluid leaving the heart again contained high levels of 6-keto-PGF1α, with lesser amounts of the other prostanoids. Addition of arachidonic acid (3 μg/ml) to the irrigating fluid caused an increase in all measured prostanoid levels, although 6-keto-PGF1α remained the predominant metabolite. In contrast, intravenous infusion of isoproterenol selectively increased the release of 6-keto-PGF1α from the irrigated heart. It is concluded that the pericardium and epicardium continuously release prostacyclin into the pericardial fluid, and that the increased release of this substance observed when cardiac workload increases derives mainly from these membranous sources. This raises the interesting possibility that pericardial prostacyclin might influence coronary vascular tone and chemoreflexes which arise from the epicardium during myocardial ischemia. 相似文献
6.
The effects of elastase on prostacyclin biosynthesis in cultured rat aortic smooth muscle cells were investigated. Prostacyclin is the major product formed from arachidonic acid by aortic smooth muscle cells. When intact cells were incubated with elastase, a significant stimulatory effect on prostacyclin biosynthetic activity in cells was evident. However, the addition of elastase directly to the cell-free homogenates did not show any effects on prostacyclin biosynthesis. The maximal effect of elastase on the stimulation of prostacyclin biosynthesis without any cellular damage was observed at a concentration of 50 unit/ml elastase. Elastase also caused a marked release of arachidonic acid. At higher concentrations of elastase (75-100 units/ml), the release of arachidonic acid and prostacyclin synthesis was observed, but, at these concentrations of elastase, cells were slightly damaged. On the other hand, the releases of prostacyclin and arachidonic acid were markedly enhanced, when cells were preincubated with elastase (1 unit/ml) for 3 days. These results indicate that elastase, even at low concentrations, causes the releases of arachidonic acid and prostacyclin, especially when aortic smooth muscle cells are pre-treated with elastase. 相似文献
7.
C.W. Karpen A.J. Merola R.W. Trewyn D.G. Cornwell R.V. Panganamala 《Prostaglandins & other lipid mediators》1981,22(4):651-661
Platelets from vitamin E-deficient and vitamin E-supplemented rats generate the same amount fo thromboxane A2 (TxA2) when they are incubated with unesterified arachidonic acid. Platelets from vitamin E-deficient rats produce more TxA2 than platelets from vitamin E-supplemented rats when the platelets are challenged with collagen. Arterial tissue from vitamin E-deficient rats generates less prostacyclin (PGI2) than arterial tissue from vitamin E-supplemented rats. The vitamin E effect with arterial tissue is observed when the tissue is incubated with and without added unesterified arachidonic acid. These data show that arterial prostacyclin synthesis is diminished in vitamin E-deficient rats. Vitamin E, , inhibits platelet aggregation both by lowering platelet TxA2 and by raising arterial PGI2. 相似文献
8.
Salvador Moncada Philip Needleman Stuart Bunting John R. Vane 《Prostaglandins & other lipid mediators》1976,12(3):323-335
Two enzyme systems and their selective inhibition are described. Microsomes from ram seminal vesicles (RSV) incubated with arachidonic acid at 22° C generated a rabbit aorta contracting substance which, after rapid ether extraction, had characteristics similar to purified standard endoperoxides. Incubation of either purified endoperoxide or the product from RSV and arachidonic acid with horse platelet microsomes (HPM) yielded a more potent rabbit aorta contracting substance characterized as thromboxane A2, with a half life of 35.9 ± 2.2 s at 37° C after ether extraction. Two inhibitors, indomethacin and benzydamine exhibited selectivity for the two enzyme systems. The IC50 for benzydamine against thromboxane synthetase was 100 μg/ml and 250 μg/ml against RSV. Indomethacin showed a greater degree of selectivity with an IC50 of 5 μg/ml for the ram seminal vesicle cyclo-oxygenase compared to 100 μg/ml for thromboxane synthetase. 相似文献
9.
J.J. Adcock L.G. Garland S. Moncada J.A. Salmon 《Prostaglandins & other lipid mediators》1978,16(2):163-177
Fragments of chopped lung from indomethacin treated guinea-pigs had an anti-aggregating effect when added to human platelet rich plasma (PRP), probably due to the production of prostacyclin (PGI2) since the effect was inhibited by 15-hydroperoxy arachidonic acid (15-HPAA, 10 μg ml?1). Both 15-HPAA (1–20 μg ml?1 min?1) and 13-hydroperoxy linoleic acid (13-HPLA, 20 μg ml?1 min?1) caused a marked enhancement of the anaphylactic release of histamine, slow-reacting substance of anaphylaxis (SRS-A) and rabbit aorta contracting substance (RCS) from guinea-pig isolated perfused lungs. This enhancement was not reversed by the concomitant infusion of either PGI2 (5 μg ml?1 min?1) or 6-oxo-prostaglandin F1α (6-oxo-PGF1α, 5 μg ml?1 min?1). Anaphylactic release of histamine and SRS-A from guinea-pig perfused lungs was not inhibited by PGI2 (10 ng - 10 μg ml?1 min?1) but was inhibited by PGE2 (5 and 10 μg ml?1 min?1). Antiserum raised to 5,6-dihydro prostacyclin (PGI1) in rabbits, which also binds PGI2, had no effect on the release of anaphylactic mediators. The fatty acid hydroperoxides may enhance mediator release either indirectly by augmenting thromboxane production or by a direct effect on sensitized cells. Further experiments to distinguish between these alternatives are described in the accompanying paper (27). 相似文献
10.
Aortic strips removed from spontaneously hypertensive (SH) rats and preincubated with arachidonic acid (1.0 X 10(-5) g/ml) for 15 min produced two times more prostaglandin (PG) like material than aortae unexposed to the precursor of PG biosynthesis. The stimulating effect of arachidonic acid was largely inhibited by indomethacin (1.0 X 10(-5) g/ml). Also, the release of PG-like material by aortic strips derived from SH rats treated with an intravenous injection of indomethacin (10 mg/kg) was inhibited by 74% compared with the control tissues. These results raised the possibility that the in vivo conversion of arachidonic acid by large arteries of SH rats may contribute to the hypotensive effect of this PG precursor in SH rats. 相似文献
11.
Lauren M. Cagen Zahir Qureshi Hiroko Nishimura 《Biochemical and biophysical research communications》1983,110(1):250-255
Saline washed red blood cells of the toadfish convert [1-14C] arachidonic acid to products that cochromatograph with prostaglandin E2 and prostaglandin F2α. This synthesis is inhibited by indomethacin (10 μg/ml). Conversion of arachidonic acid to prostaglandin E2 was confirmed by mass spectrometry. When saline washed toadfish red blood cells were incubated with a mixture of [1-14C]-arachidonic acid and [5,6,8,9,11,12,14,15,-3H]-arachidonic acid, comparison of the isotope ratios of the radioactive products indicated that prostaglandin F2α was produced by reduction of prostaglandin E2. The capacity of toadfish red blood cells to reduce prostaglandin E2 to prostaglandin F2α was confirmed by incubation of the cells with [1-14C] prostaglandin E2. 相似文献
12.
Acute arthritis was induced by injection of cell-free extract of group A Streptococci into the knee joints of mature male rats. Slices of control and inflamed synovia were incubated for 30 to 240 minutes and the rate of prostaglandin E (PGE) released into the medium was measured by radioimmunoassay. PGE release from inflamed synovia was 5–8 fold higher than that in normal tissue. Incubation of inflamed synovia with corticosterone acetate, dexamethasone or prednisone (100 μg/ml) for one or four hours reduced PGE release by 33% and 55% respectively. Lower concentrations of corticosterone (10 – 30 μg/ml) were ineffective. Aldosterone and progesterone (100 μg/ml) had no effect on PGE release throughout the incubation period. Chloroquine (10 μg/ml) inhibited PGE release from inflamed synovia by 50%. Indomethacin (1 μg/ml) abolished PGE release by 90%. Corticosterone, dexamethasone and prednisone reduced PGE content of inflamed synovia by approximately 45% during a 4-h incubation period. Aldosterone and progesterone were ineffective, while indomethacin reduced PGE content by 70%. The suppressive action of corticosterone on PGE release was prevented by addition to the medium of arachidonic acid (2 μg/ml). By contrast, the inhibitory action of indomethacin was not affected by provision of exogenous substrate. We suggest that glucocorticosteroids reduce PGE release by limiting the availability of the substrate for prostaglandin biosynthesis, and this may well explain some of their anti-inflammatory properties. 相似文献
13.
Modulation of Platelet thromboxane A2 and arterial prostacyclin by dietary vitamin E 总被引:1,自引:0,他引:1
Platelets from vitamin E-deficient and vitamin E-supplemented rats generate the same amount of thromboxane A2 (TxA2) when they are incubated with unesterified arachidonic acid. Platelets from vitamin E-deficient rats produced more TxA2 than platelets from vitamin E-supplemented rats when the platelets are challenged with collagen. Arterial tissue from vitamin E-deficient rats generates less prostacyclin (PGI2) than arterial tissue from vitamin E- supplemented rats. The vitamin E effect with arterial tissue is observed when the tissue is incubated with and without added unesterified arachidonic acid. These data show that arterial prostacyclin synthesis is diminished in vitamin E-deficient rats. Vitamin E, in vivo, inhibits platelet aggregation both by lowering platelet TxA2 and by raising arterial PGI2. 相似文献
14.
P G de Groot H J Brinkman M D Gonsalves J A Van Mourik 《Biochimica et biophysica acta》1985,846(3):342-349
Prostaglandin synthesis in endothelial cells may be initiated by the addition of exogenous substrate (arachidonic acid) or by addition of thrombin or the CA2+-ionophore A23187, which leads to prostacyclin formation from endogenous substrates. We noticed that endothelial cells produce more than twice the amount of prostacyclin when incubated with thrombin and arachidonic acid together than with arachidonic acid alone. In addition, it was found that the thrombin-induced conversion of endogenous substrates was inhibited by exogenous arachidonic acid. This means that the conversion of exogenous added arachidonic acid to prostacyclin was stimulated by thrombin. This activation of the enzymes involved in prostacyclin synthesis lasted about 5 min and could be inhibited by phospholipase inhibitors such as mepacrine and p-bromophenyl-acylbromide but not by the cAMP analogue dibutyryl cAMP, an inhibitor of arachidonic acid release from cellular phospholipids. These data demonstrate that, in addition to causing release of endogenous substrate, thrombin and the Ca2+-ionophore also activate the enzyme system involved in the further transformation of arachidonic acid. 相似文献
15.
Prostaglandin F2α (PGF2α) release by luteal tissue from mares was quantified to determine if exogenous prostaglandin analog increased endogenous luteal PGF2α production during induced luteolysis. On day 8 after ovulation, luteal tissue was collected by flank laparotomy and endometrium was collected by uterine biopsy. Mares were assigned to one of four treatments: (1) no intramuscular injection at 0-hr (n = 5), (2) 250 μg Fluprostenol (ICI 81008 PGF2α analog) at 4-hr (n = 4), (3) 250 μg Fluprostenol at 12-hr (n = 5), or (4) 250 μg Fluprostenol at 28-hr (n = 5) prior to tissue collection at laparotomy. Blood was collected from a jugular vein at laparotomy. Luteal and endometrial tissues (100-mg minces) were incubated in duplicate in 5 ml of Krebs-Ringer bicarbonate buffer (pH 7.4) in an ice bath in an air atmosphere or at 37°C in an atmosphere of 95% O2:5% CO2. The incubation treatments consisted of: no treatment, indomethacin 1.3 × 10?4M, 1 μg/ml of arachidonic acid, 10 μg/ml of Fluprostenol, and 100 μM dbc-AMP (Fluprostenol was not added to endometrial tissue incubations). The injection of Fluprostenol induced luteolysis in these mares as indicated by decreased plasma progesterone and luteal tissue progesterone production (P<0.01). Luteal PGF2α production was only detectable in tissue from mares that had been injected with Fluprostenol; production reached a maximum by 12 hr post-injection and had returned to pre-treatment levels by 28 hr (P<0.01). Endometrial tissue produced PGF2α, but this activity was not significantly affected by injection of mares with Fluprostenol. Increased production of PGF2α by luteal tissue of mares during PGF2α analog induced luteolysis was similar to that observed in the pig and ewe. 相似文献
16.
《Prostaglandins, Leukotrienes and Medicine》1984,13(2):179-196
Normal human endometrium (classified by histology and date after last menstrual period) was cultured for 72h, and the output of prostaglandin F2α and 6-oxo-prostaglandin Fla detected by radioimmunoassay. Hormones/stimuli were added to the culture during the second day of culture for 5h and 19h periods.
- 1.1) The output of prostaglandin F2α from cultured endometrium was significantly higher (p<0.05) at the beginning (d4–8) and end (d25–30) of the menstrual cycle, compared to mid-cycle (d13–24) endometrium. Significantly more prostaglandin F2α was released from proliferative than from secretory phase endometrium (p<0.02).
- 2.2) Prostaglandin F2α release was rapidly stimulated by sodium arachidonate (20–300 μg/ml), and by calcium ionophore A23187 (5 μg/ml) at an extracellular calcium ion concentration of 1.8mM.The ionophore stimulation was greater in mid-cycle endometrium than in endometrium from the beginning or the end of the menstrual cycle.
- 3.3) Estradiol-17β (10 ng/ml) gradually increased the output of prostaglandin F2α from secretory phase endometrium, and this stimulation was observed in the post-incubation period after hormone had been removed from the incubation medium.
- 4.4) Oxytocin (1 × 10−5U/ml caused a more rapid stimulation of prostaglandin F2α output from secretory phase tissue (p<0.05 during the first 5h incubation period with hormone).
- 5.5) Oxytocin (1 × 10−5 U/ml) and estradiol (long/ml) together significantly stimulated prostaglandin F2a production by proliferative as well as secretory phase endometria.
- 6.6) A high dose of hydrocortisone (loo μg/ml) inhibited the output of prostaglandin F2α from proliferative and secretory phase endometrium and also from ionophore-stimulated endometrium. However, this dose of hydrocortisone did not inhibit the synthesis of prostaglandin F2a from exogenous arachidonic acid, or the estradiol-induced increase in prostaglandin F2α production.
- 7.7) Co-culture of endometrium with myometrium did not modify the output of prostaglandin F2α or of 6-oxo-prostaglandin Fla from cultured tissues.
- 8.8) These experiments suggest that arachidonic acid supply to the cyclooxygenase enzyme may vary during the menstrual cycle: and indicate a gradual increase in prostaglandin synthesising capacity in response to estrogen, more rapid control via oxytocin, and an interaction between estrogen and oxytocin to modulate prostaglandin F2a synthesis in human endometrium.
17.
Isolated rat aortae were incubated at 22°C in tris-buffered saline (pH 7.4). The incubation medium was changed every 10 min, and the amounts of prostacyclin (PGI2) in the medium were immediately bioassayed as an inhibitory activity against rabbit platelet aggregation induced by ADP. The addition of arachidonic acid to the medium increased the generation of PGI2 but this was followed by a gradual decrease even in the presence of the same amount of arachidonic acid. The decrease of PGI2 generation from exogenous arachidonic acid was prevented by tryptophan, which is required by PG hydroperoxidase with heme compound as cofactors. MK-447 and its analogues, which are phenolic compounds and exerted tryptophan-like action on the PG endoproxide biosynthesis by bovine seminal vesicle microsomes, also prevented the decrease of PGI2 generation in isolated rat aortae. The phenolic compounds enhanced PGI2 generation from endogenous arachidonic acid. These results indicate that theh phenolic compounds enhanced PGI2 generation in vascular tissue, acting as a tryptophan-like cofactor of PG hydroperoxidase. 相似文献
18.
In isolated canine atrium, perfused with blood from a donor dog, the infusions of both prostaglandins (PG)I2 and E2 (0.1–1 μg/min) into the sinus node arterial cannula neither altered the sinus rate and developed tension nor the positive chronotropic and inotropic responses elicited by either electrical stimulation or by injected norepinephrine. Infusion of arachidonic acid (10–100 μg/min), a precursor of PGs, or indomethacin (15–20 μg/min), an inhibitor of PG synthesis, into the sinus node arterial cannula also failed to alter the increase in sinus rate or developed tension produced by either adrenergic stimulus in the isolated atria. When arachidonic acid, 100–300 μg/kg or PGI2, 1 μg/kg, were injected into the jugular vein of the donor dog, they produced a fall in systemic blood pressure; this effect of arachidonic acid but not of PGI2 was abolished by indomethacin, 1 mg/kg. During administration of either arachidonic acid or indomethacin to the donor dog, the positive chronotripic and inotropic responses to adrenergic stimuli in the isolated atria also remained unaltered. These data indicate that PGs do not modulate adrenergic transmission in the blood perfused canine atrium. 相似文献
19.
《Prostaglandins and medicine》1978,1(1):39-48
Acute arthritis was induced by injection of cell-free extract of group A type 4 Streptococci, into the knee joints of three month old male rats. Slices of the inflamed synovium obtained from these rats were incubated for 60–240 minutes, and the rate of prostaglandin E accumulation in the medium was measured by radioimmunoassay.Prostaglandins of the E type accumulated in the medium at a near linear rate during the incubation of the inflamed synovium for 4 hours. Incubation of inflamed synovium in the presence of colchicine (10 μg/ml) brought about a two-fold increase in the prostaglandin E accumulation in the medium after a latency of one hour. Tissue content of prostaglandin E after 4 hours of incubation of inflamed synovium with colchicine doubled as well. In contrast, incubation of inflamed synovium with chloroquine (10 μg/ml), corticosterone or dexamethasone (100 μg/ml each) reduced prostaglandin E accumulation in the medium by 50% at 1–4 hours. Likewise, chloroquine, corticosterone or dexamethasone reduced the tissue content of prostaglandin E in the inflamed synovium after 4 hours of incubation. The suppressive action of chloroquine was prevented by addition to the medium of arachidonic acid (2 μg/ml).It is concluded that the anti-inflammatory properties of colchicine are probably not related to prostaglandin biosynthesis. On the other hand chloroquine exerts its anti-inflammatory properties by curtailing substrate availability (arachidonic acid) for prostaglandin production, similarly to the anti-inflammatory mechanism of steroid hormones. 相似文献
20.
PGA1 and PGA2 (10, 100 μg/ml) significantly increased human adrenal cAMP levels and cortisol output but low doses (1 μg/ml) depressed both parameters. Only 1 μg/ml PGA1 significantly increased aldosterone output while higher doses depressed same. The low PGA2 dose (1 μg/ml) depressed aldosterone output. The glucocorticoid and mineralocorticoid outputs appear to be inversely modulated by prostaglandins. PGB1 and PGB2 behaved similarly to E type prostaglandins. However, like PGA1, 1 μg/ml of PGB1 or PGB2 significantly increased aldosterone output. Higher doses were ineffective. The present findings reveal an increased complexity of prostaglandin modulation of cyclic nucleotides and steroid output. 相似文献