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1.
Prostaglandin F2α (PGF2α) (1–100 ng) and acetylcholine (ACh) (0.3–30 μg) injected selectively into the artery supplying the submaxillary gland of the dog produced salivation and an increase in blood flow. Both salivary and vascular responses to PGF2α developed slowly and lasted long as compared with those to ACh. On a weight basis PGF2α was about 1000 times more potent than ACh in producing salivation. Upon repeated injections of PGF2α most glands developed moderate desensitization to PGF2α but not to ACh. Both salivary and vascular responses to PGF2α were abolished by infusion of tetrodotoxin ( or 0.1 or 0.2 μg/min), whereas those to ACh remained virtually unchanged. These results indicate that in the dog submaxillary gland PGF2α causes salivation and vasodilation exclusively through excitation of the parasympathetic postganglionic neurons. 相似文献
2.
Mildred E.D. Cerini W.A. Chamley J.K. Findlay J.R. Goding 《Prostaglandins & other lipid mediators》1973,3(4):399-404
The luteotrophic properties of LH were examined by determining whether this hormone could overcome the luteolytic action of Prostaglandin F2α (PGF2α) .Sheep with ovarian autotransplants were given intra-arterial infusions of LH (10 μ g/h for 6 h). PGF2α (5 μ g/h) was then added to the infusate and the infusion continued for 6 hours. In all cases, LH failed to counteract the effect of PGF2α and luteolysis resulted. 相似文献
3.
The following experiments were designed in order to examine the inter-relationships of various prostaglandins (PG's) and the adrenergic nervous system, in conjunction with blood pressure and heart rate responses, . Stimulation of the entire spinal cord (50v, 0.3–3 Hz, 1.0 msec) of the pithed rat increased blood pressure, heart rate and plasma epinephrine (EPI) and norepinephrine (NE) concentration (radioenzymatic-thin layer chromatographic assay). Infusion of PGE2(10–30 μg/kg. min, i.v.) suppressed blood pressure and heart rate responses to spinal cord stimulation while plasma EPI (but not NE) was augmented over levels found in control animals. PGI2 (0.03–3.0 μg/kg. min, i.v.) suppressed the blood pressure response to spinal cord stimulation without any effect on heart rate or the plasma catecholamine levels. PGE2 and PGF2α(10–30 μg/kg. min, i.v.) did not change the blood pressure, heart rate or plasma EPI and NE responses to the spinal cord stimulation although PGF2α disclosed an overall vasopressor effect during the pre-stimulation period. At the pre-stimulation period it was also observed that PGE2, PGF2α and PGI2, had a positive chronotropic effect on the heart rate, the cardiac accelerating effect of PGE2 was not abolished by propanolol. These studies suggest that in the rat, PGE2 and PGI2 modulate sympathetic responses, primarily by interaction with the post-synaptic elements — PGE2 on both blood vessels and the heart and PGI2 by acting principally on blood vessels. 相似文献
4.
Differential effects of tetrodotoxin on the sialogenous and vasodilator actions of prostaglandin E2 in the dog salivary gland 总被引:1,自引:0,他引:1
Prostaglandin E2 (PGE2) (0.1–300 nmol) and acetylcholine (ACh) (0.3–300 nmol) were injected into the glandular artery through which the mandibular gland of the dog was perfused with blood at a constant pressure of about 100 mm Hg. Either substance produced salivary secretion and an increase in blood flow rate in a dose-related manner. The effects of PGE2 were far more powerful and long-lasting than those of ACh. The potency of PGE2 was about 1/300 that of prostaglandin F2α on a molar basis in producing the two effects. During complete nerve-block attained by intra-arterial infusion of tetrodotoxin (0.3 nmol/min) the sialogenous action of PGE2 was abolished, although not completely, whereas the vasodilator effect remained in larger part. Both sialogenous and vasodilator effects of ACh were not affected by tetrodotoxin. These results indicate that the sialogenous effect of PGE2 was due in most part to a neural, probably parasympathetic, excitant action, whereas the vasodilator action was due in larger part to a direct one on the vasculature. 相似文献
5.
Five healthy adult men received iv PGF2α at dosages of 0.05, 0.20 and 2.0 μg/kg/min for 30 min. There were no significant changes in serum FSH, LH or TSH levels. Serum GH and cortisol levels were slightly increased at the highest dosage. These responses were associated with, and presumably a result of, stressful side effects. Thus, PGF2α cannot be used as a provocative test of pituitary hormone reserve.Prostaglandins (PG's) have recently been implicated in the release of a number of hormones from the anterior pituitary gland. The stimulation of GH release by PG's of the E series from incubated rat pituitary slices has been demonstrated. stimulation by PGE1 of ACTH in rats and of GH release in man has also been shown.The present study was undertaken in order to examine the efficacy of iv administration of PGF2α as a provocative test of anterior pituitary hormone reserve in man. The responses in circulating levels of gonadotropins, TSH, GH, and cortisol (as an index of ACTH) were measured. 相似文献
6.
At low concentrations (i.e., 10?12–10?9 mol/l), PGF1α and PGF2α very intensely stimulated both the DNA-synthetic and mitotic activities of hepatocytes in 4-day-old primary cultures of neonatral rat liver. DNA replication was more intensely enhanced by PGF2α than by PGF1α, whereas mitotic activity was nearly equally affected by the two prostaglandins. On the whole, the growth-promoting activity of PGF1α used by itself or in equimolar mixtures with other prostaglandins (. ., A1, E1, .) mimicked that of arachidonic acid we previously reported (1). On a molar basis, PGF2α by itself stimulated hepatocytes′ DNA synthesis is more powerfully than arachidonate did, and when used in equimolar mixtures with other prostaglandins was at least as potent as arachidonic acid. These observations establish prostaglandins of the F series as quite powerful commitment factors and, though by a lesser degree, also intracycle regulators for neonatal rat hepatocytes in primary culture. However, the understanding of the role(s) of prostaglandins of F and other series in the physiological control of hepatocytes′ proliferative activation must wait the clarification of their interaction(s) with other arachidonate derivative(s) and polypeptide growth factor(s) which also may be involved in the process. 相似文献
7.
Effect of prostaglandin E2 on vascular responses of the rabbit kidney to nerve stimulation and noradrenaline, in vitro and in situ 总被引:2,自引:0,他引:2
The effect of prostaglandin E2 on vascular responses of the rabbit kidney to renal nerve stimulation and noradrenaline was examined and as a test of the hypthesis that prostaglandins of the E series may be involved in the regulation of adrenergic neuroeffector transmission. Intraarterial administration of prostaglandin E2 to the kidney caused marked inhibition of vascular responses to nerve stimulation whereas the responses to noradrenaline were not significantly altered. In the preparation, vascular responses to both nerve stimulation and noradrenaline were inhibited by prostaglandin E2 infusion, although its effect on responses to nerve stimulation was approximately twice that observed on responses to noradrenaline.It is concluded that prostaglandin E2 acts primarily at a prejunctional level of adrenergic neuroeffector transmission in the kidney, although a postjunctional effect has also been observed. 相似文献
8.
The rate of disappearance of total circulating radioactivity following an intravenous bolus injection of 3HPGF2α was determined during splanchnic artery occlusion (SAO) shock in the dog. In addition, the pattern of PGF2α metabolite formation was assessed in both shocked and nonshocked animals. Although the clearance of circulating prostaglandin metabolites is significantly impaired during SAO shock as a result of decreased renal function, neither the pattern nor the time course of PGF2α metabolite formation appears to be altered. Thus, increases in circulating prostaglandin concentrations during SAO shock reflect an increase in the rate of synthesis and release of these materials, and are not the result of decreased prostaglandin degradation. 相似文献
9.
L. Hamberger L. Nilsson B. Dennefors I. Khan A. Sjögren 《Prostaglandins & other lipid mediators》1979,17(4):615-621
Human corpora lutea of defined ages were excise at operation cut into pieces and incubated in the presence of HCG, PGF2α and PGE2 alone or in combination. Following incubation cAMP formation in tissue and medium was determined. HCG-stimulated tissue cAMP content was most pronounced at a corpus luteum age of 7–10 days after ovulation. This stimulation was antagonized by PGF2α in corpora lutea older than 6 days. PGE2 stimulated cAMP formation and this effect was more pronounced when HCG and PGE2 were combined. A possible role for PGF2α as a luteolytic substance in the human is suggested. 相似文献
10.
The effects of 19-hydroxy-prostaglandins (19-OH-PGs) were tested on the rabbit oviduct and uterus and on the rhesus monkey () uterus. The 19-OH-PGEs suppressed spontaneous oviductal and uterine activity in the rabbit. The qualitative effect on the rabbit oviduct of 19-OH-PGEs was similar to that of PGE2. However, the typical response of the rabbit uterus to PGE2 was an increase in muscle activity. With regard to the rabbit oviduct, 19(R)-OH-PGE2 was as potent as PGE2, but 19(S)-OH-PGE2 was approximately as potent as PGE2. Based on the dose of 19-OH-PGEs usually required to cause a minimal suppression and the dose of PGE2 required to cause a minimal stimulation of rabbit uterine activity, 19(R)-OH-PGE2 was twice as potent as PGE2 while 19(S)-OH-PGE2 was as potent as PGE2. Stimulatory effects on the rabbit oviduct and uterus were observed following administration of 19-OH-PGEs and PGF2α. The potency on the rabbit oviduct of 19(S)-OH-PGF2α was about to that of PGF2α; the potency of 19(R)-OH-PGF2α was about to that of PGF2α. Both 19-OH-PGFs were approximately to as potent as PGF2α on the rabbit uterus. At the doses tested 19-OH-PGFs were inactive on the monkey uterus. Thus, these compounds are at least as active as PGF2α. In contrast, 19(R)-OH-PGE2 had approximately the same potency as PGE2 in stimulating monkey uterine activity; but 19(S)-OH-PGE2 was approximately as potent as PGE2. 相似文献
11.
W. Schramm L. Bovaird M.E. Glew G. Schramm J.A. McCracken 《Prostaglandins & other lipid mediators》1983,26(3):347-364
In view of the pulsatile nature of PGF2α secretion from the ovine uterus at the time of luteolysis, experiments were designed to examine the effect of pulsed infusions of PGF2α on luteal function and to re-examine the minimal effective levels of PGF2α required to induce luteolysis. To mimic physiological conditions, hour-long infusions of PGF2α in increasing concentrations were given either 4 times in 19 h or 5 times in 25 h into the arterial supply of the autotransplanted ovary in conscious sheep on day 12 of an induced cycle. Blood flow and progesterone secretion rate from the ovary were used to monitor directly the luteolytic effect of administered PGF2α. The concentration of LH in peripheral plasma was measured throughout each infusion experiment and the presence of a preovulatory peak of LH was used as an indicator of the permanence of luteal regression. Four pulses of PGF2α in 19 h caused complete corpus luteum regression in only 1 of 4 animals whereas the addition of a fifth pulse (5 pulses in 25 h) caused permanent regression in 4 out of 4 animals. Infusion of 5 hour-long pulses of saline or PGF2α at a rate of <0.04 μg/h did not induce permanent suppression of progesterone secretion. The average total effective dose of PGF2α required to induced luteal regression when given as 5 pulses was 1/40th of the amount currently regarded as the minimal effective one when given by constant infusion into the ovarian artery. In another series of experiments the luteolytic effect of a single hour-long pulse of 0.1 μg/h PGF2α given daily for either 3 or 4 days was investigated. A significant fall (ANOVA, F0.01) in progesterone secretion rate, which reached a nadir at , was followed by a recovery of progesterone secretion rate. Permanent luteal regression did not occur with this protracted regimen, suggesting that a relatively short pulse frequency of PGF2α over a minimal period of 24 h is a necessary condition for physiological regression of the corpus luteum in sheep. 相似文献
12.
Using an intrauterine pressure transducer to telemeter uterine pressure a method has been devised to assess the sensitivity of the uterus to intra-aortic PGF2α infusions. Intra-aortic infusion of 1–10 μg PGF2α/min into the 21–24 Day Pregnant rabbit has little effect on uterine contractility. A continuous intra-aortic infusion of 1 μg PGF2α/h was found to result in a gradual increase of sensitivity to PGF2α even after cessation of the continuous infusion. 相似文献
13.
We have compared the production of prostaglandins in fibroblast-like cells and endothelial cells in culture. Of the fibroblasts studied , SHE, BP6T and KD produce significant amounts of PGI2, PGE2 and PGF2F2 under optimal culture conditions, but only 3T3 and BHK produce TxA2 in addition to PGI2. The adult bovine aortic endothelial cells (ABAE) and fetal bovine heart endothelium (FBHE) synthesise PGI2 but not TxA2, either from endogenous or exogenous substrates. Both cultured endothelial cells and fibroblasts apparently lack 15-hydroxyprostaglandin dehydrogenase pathway and the ability to convert 6-Keto PGF1α into 6-Keto PGE1. PGI2 production by ABAE was 3–5 times that of FBHE, about twice that of SHE cells and 6–8 times that of or BP6T cells. Supernatants or media obtained from these cells inhibited aggregation of human platelet-rich plasma, a known biological effect of PGI2. This effect was abolished when cell monolayers were preincubated with indomethacin or tranylcypromine. RIA and chromatographic data of 6-Keto PGF1α from these experiments confirmed that the inhibition of platelet aggregation was due to the formation of PGI2. The production of all prostanoids by endothelial cells or fibroflasts was significantly higher during the exponential phase of growth as compared to confluent monolayers. We propose that fibroblasts or SHE can serve as useful experimental models for the study of metabolism and transport of PGI2 and/or TxA2 in cells of nonendothelial nature. 相似文献
14.
The frequency of spontaneous contractions of seminiferous tubules of the rat appeared to be increased in a dose-dependent manner by prostaglandin F1α. PGF1α treatment increased the tonus of the smooth muscle cells in the wall of the tubules as indicated by a reduction in the diameter of the tubules. When the tubules were rinsed successively with fresh Tyrode's solution, the contractile frequency was diminished. Returning the original bathing medium to the tubules restored their contractile frequency, as did treatment of the rinsed tubules with PGF1α (10-7 M). Pre-injecting the rats with indomethacin tended to reduce the contractile frequency of the extirpated tubules. Treating the tubules with a solution of indomethacin for 90 min. was more effective than pretreatment in reducing contractile frequency, but a combination of these two procedures produced the greatest inhibition. PGF1α restored the contractile frequency of the indomethacin-treated tubules. Our results indicate that PGs modulate the contractility of the tubules. 相似文献
15.
John W. Wilks Kristi K. Forbes Jerome F. Norland 《Prostaglandins & other lipid mediators》1973,3(4):427-437
Prostaglandin F2α (PGF2α) did not alter the biosynthesis of progesterone by slices of luteinized rat ovaries when used in concentrations from 1 to 10,000 ng/ml of incubation medium; likewise, PGF2α did not affect the incorporation of acetate-1-14C into progestins. PGF1α, 15-keto PGF2α, and PGE1 did not alter the biosynthesis of progesterone by luteinized rat ovaries; PGE2 inhibited the production of progesterone when used at a concentration of 10 μg/ml, but not at lower doses. PGF2α in combination with luteinizing hormone (LH) enhanced the metabolism of progesterone to 20α-hydroxypregn-4-en-3-one in luteinized rat ovaries. Interestingly, PGF2α, at a high concentration of 10 μg/ml, did stimulate progesterone biosynthesis by slices of ovarian tissue from immature rats hormonally primed to simulate “pseudopregnancy,” suggesting a steroidogenic action of prostaglandins on the ovarian follicular or interstitial cell. PGF2α (10 μg/ml) did not stimulate the biosynthesis of progesterone or 20α-hydroxypregn-4-en-3-one by slices of rabbit corpora lutea or rabbit ovarian interstitial tissue. It is concluded that prostaglandins do not stimulate progestin biosynthesis in rat luteal tissue. 相似文献
16.
An investigation of the effect of PGF2α induced parturition alone or in combination with neostigmine (NEO) on subsequent productivity was conducted in a total confinement swine production unit. Forty-five crossbred gilts and 106 sows were randomly assigned to one of six treatments: (1) , (2) , (3) , (4) , (5) , (6) . PGF2α injections (IM) were given 2 days prior to the mean expected farrowing day for this farm (day 112). NEO injections (IM) were given after the fourth pig born in gilt litters and after the fifth pig born in sow litters. Females injected with 0 or 10 mg PGF2α farrowed 71.7 ± 3.7 and 31.4 ± 3.4 hours after treatment, respectively (P<0.01). No other parameters measured were significantly affected by injection of PGF2α. These data show that PGF2α effectively induced parturition and did not adversely affect subsequent litter productivity. NEO was found to be ineffective in reducing total farrowing time (P>0.05). 相似文献
17.
Alam Farzad Neal S. Penneys Abdul Ghaffar Vincent A. Ziboh Jean Schlossberg 《Prostaglandins & other lipid mediators》1977,14(5):829-837
The biosynthesis of PGE2 and PGF2α was measured in intact peritoneal exudate preparations obtained fom -treated and control C3H mice. Although both the control and stimulated preparations biosynthesized PGF2α and PGE2 from [1–14C] arachidonic acid, the stimulated preparations generated more of both prostaglandins than did nonstimulated preparations, probably as a result of increased synthesis within macrophages. Increased transformation of PGE2 into PGF2α 9-ketoreductase was noted in stimulated preparations when compared to that in control cells. The data suggest that stimulated macrophages are capable of generating increased quantities of PGF2α and therefore might function as one source of this substance in resolving inflammatory reactions. 相似文献
18.
The activity of prostaglandins (PG) in producing vascular permeability was quantitated by dye extraction method in skin of anaesthetized rabbits. PGE1 and PGE2 (0.01–10 μg) produced increase in vascular permeability. Activity was approximately equal to that of histamine (Hist) and of that of bradykinin (BK) on a weight basis. The activity of PGF1α and PGF2α was only of that of PGE1 or PGE2.In spite of the relatively low potency of PGE1 and PGE2 in the rabbit, near threshold doses (0.1 or 1 μg) of PGE2 could potentiate permeability responses to bradykinin (0.1 μg) by 10 or 100-fold, respectively. Equivalent doses (0.1 or 1 μg) of histamine could not potentiate the bradykinin responses. Arachidonic acid (AA) at 1 μg, produced a 10-fold potentiation in the permeability response to bradykinin (0.1 μg). Pretreatment of the rabbits with indomethacin (20 mg/kg, i.p.) reduced the responses of BK (0.1 μg) + AA (1 μg) down to a similar magnitude of those seen with bradykinin alone. However, indomethacin did not block responses to either, BK alone, BK + PGE2, or BK + Hist. Various doses (1, 10, 100 and 300 μg) of arachidonic acid alone also produced increase in cutaneous vascular permeability, although its potency was only – of that of PGE2. This activity of arachidonic acid was attributed in part to its bioconversion to PGE2, since its activity was significantly reduced by the prostaglandin antagonist, diphloretin phosphate (DPP) (60 mg/kg, i.v.) and by indomethacin (20 mg/kg, i.p.), which blocks conversion of arachidonic acid to prostaglandins. Arachidonic acid may owe some of its permeability increaseing effects to histamine release, since its effects were also reduced by the antihistamine, pyrilamine (2.5 mg/kg, i.v.). 相似文献
19.
Edwin K. Jackson Howard D. Uderman William A. Herzer Robert A. Branch 《Life sciences》1984,35(2):221-228
The purpose of this study was to determine the effects of chronic administration of the thromboxane synthetase inhibitor, UK 38,485, on noradrenergic neurotransmission. Male Sprague Dawley rats (n=14) were treated once daily with either UK 38,485 (100 mg/kg; n=7) or the vehicle of UK 38,485 (olive oil; n=7) by gavage. The dose of UK 38,485 chosen was sufficient to inhibit platelet TXB2 production by >90% for 24 hours. One week into the treatment animals were prepared for perfusion of their mesenteric vascular beds. Vasoconstrictor responses to both exogenous norepinephrine and periarterial nerve stimulation were determined both before and during an infusion of angiotensin II (9ng/min) into the superior mesenteric artery. UK 38,485 significantly (P<0.02) attenuated the vascular response to periarterial nerve stimulation without altering the vascular response to either norepinephrine or angiotensin II. UK 38,485 did not influence the baseline perfusion pressure, the mean arterial blood pressure or the potentiation of neurotransmission by angiotensin II. These data indicate that in the rat mesentery UK 38,485 attenuates the release of neurotransmitter from sympathetic nerve terminals. 相似文献
20.
Charles R. Wallace Terry E. Kiser George B. Rampacek Robert R. Kraeling 《Prostaglandins & other lipid mediators》1985,30(6):925-933
Half-life (), volume of distribution (Vd)_and total body clearance (TBC) of 13, 14-dihydro-15-keto PGF2α (PGFM) were measured in order to determine optimal sampling frequency for accurate measurement of PGFM. Three yearling Holstein bulls (349.2 ± 6.7 kg) and 3 yearling Holstein steers (346.7 ± 7.0 kg) were utilized in a 3 × 3 Latin square design. Animals were given 0, 25 or 50 μg PGF2α I.V.; blood samples collected every 2 min and plasma PGFM determined. The , Vd and TBC of PGFM were 2.3 ± .2 min, 43.3 ± 3.3 liters and 13.7 ± 1.9 liters/min, respectively and were similar for 25 and 50 μg doses. To determine the relationship between endogenous PGFM and LH secretion in bulls, blood samples were collected every 2 min for 12 h in 4 yearling Angus bulls (489.1 ± 11.6 kg). All animals elicited at least one LH surge and PGFM concentrations were measured in samples coincident with the LH surge. Mean plasma PGFM concentrations were greater prior to the LH surge than during the LH surge. In addition, mean plasma PGFM concentration and frequency of PGFM peaks appeared to increase prior to the LH surge suggesting an association between PGFM and pulsatile LH secretion in the bull. 相似文献