首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献,搜索用时 46 毫秒
1.
Prostaglandin E2 (PGE2) has previously been shown to inhibit sympathetic neurotransmission in different organs and species. Based on this inhibitory effect and on its reversal by cyclo-oxygenase inhibitors, PGE2 has been claimed to be a physiological modulator of in vivo release of norepinephrine (NE) from sympathetic nerves. It is now recognized that prostacyclin (PGI2) is the main cyclo-oxygenase product in the heart. We therefore addressed the question whether PGI2, within the same preparation, is formed in increased amounts during sympathetic nerve stimulation and has neuromodulatory activity.The effluent from isolated rabbit hearts subjected to sympathetic nerve stimulation or to infusion of NE or adenosine (ADO) was collected, and its content of PGE2 and 6-keto-PGF (dehydration product of PGI2) was analyzed using gas chromatography/mass spectrometry, operated in the negative ion/chemical ionization mode. Other hearts were infused with PGI2 and nerve stimulation induced outflow of endogenous NE into the effluent was analyzed using HPLC with electrochemical detection. Nerve stimulation at 5 or 10 Hz (before but not after adrenergic receptor blockade), as well as infusion of NE (10−6–10−5M) or ADO (10−4M) increased the cardiac outflow of 6-keto-PGF1α. Basal and nerve stimulation induced efflux of 6-keto-PGF1α was approximately 5 times higher than the corresponding efflux of PGE2. PGI2 dose-dependently inhibited the outflow of NE from sympathetically stimulated hearts, the inhibition at 10−6M being approximately 40%.On the basis of these observations we propose that PGI2 is a more likely candidate than PGE2 as a potential modulator of neurotransmission in cardiac tissue in vivo.  相似文献   

2.
Sympathetic nerve stimulation of the perfused mesenteric arterial bed of the rabbit, , increase the secretion of prostaglandin (PG)I2 and PGE2. Prazosin (4.8 × 10−6), and α1 adrenergic receptor antagonist, inhibited this inrease in release of PGI2 but not of PGE2 whereas rauwolsin (10−7 M), an α2 adrenergic receptor antagonist, inhibited the increase in release of PGE2 but not of PGI2. Prazosin (10−6 M) completely blocked the vasoconstrictor response to nerve stimulation, and to norepinephrine and phenylephrine administration, suggesting there to be little of an α2 adrenergic receptor component in this response. It is concluded that the increase in PGI2 release follows the activation of α1 adrenergic receptors and is therefore post-junctional in origin, whereas the increase in PGE2 release follows the activation of α2 adrenergic receptors and may be pre- and/or post-junctional in origin.Indomethacin (2.8 × 10−7, 5.6 × 10−7 and 1.12 × 10−6 M did not affect the vasoconstrictor responses to nerve stimulation at 10 Hz, whereas rauwolsin (10−7 M) in the presence of indomethacin substantially increased them. These results indicate that PGE2 does not regulate norepinephrine release following nerve stimulation at 10 Hz to rabbit mesenteric arteries, and that the inhibition of norepinephrine release following stimulation of α2 pre-junctional receptors is independent of PG involvement.  相似文献   

3.
In the Tyrode's perfused rabbit kidney PGI2 (1.3 × 10−8-3.3 × 10−7M) dose-dependently inhibited vasoconstrictor responses to sympathetic nerve stimulation, as did PGE2. The dose-effect curve of the two compounds differed, making PGI2 the less potent in the low concentration and the more potent in the high. PGI2 also inhibited the vasoconstrictor response to exogenous noradrenaline, but it had no effect on transmitter release. The main metabolite of PGI2, 6-keto-PGF, was ineffective both on noradrenaline release and on vascular responses to nerve stimulation or exogenous noradrenaline. It is suggested that PGI2,if a significant renal prostaglandin, may modulate renal neuroeffector transmission post-junctionally, thereby forming a complement to the prejunctional action of PGE2.  相似文献   

4.
Isolated rabbit hearts were infused with 14C-arachidonic acid and subjected to sympathetic nerve stimulation. Prostaglandins in the cardiac effluent were extracted and separated using thin layer chromatography. Other hearts were infused with un-labelled arachidonic acid and the effluent was assayed for neurosecretion inhibitory capacity on the field-stimulated guinea pig vas deferens, and for anti-aggregatory activity on ADP-induced platelet aggregation. PGs in the effluent from hearts infused with un-labelled arachidonic acid were extracted and separated on TLC, and the different fractions were assayed for neurosecretion inhibitory activity.Sympathetic nerve stimulation after preincubation with 14C-AA elicited outflow of four different peaks of 14C-labelled PGs: one chromatographing close to PGF (probably mainly 6-keto-PGF), and three peaks corresponding to PGA2/PGB2, PGD2, and PGE2 respectively. The cardiac interstitial effluent contained anti-aggregatory material which was inactivated by heat treatment, and thus probably identical to PGI2. The cardiac effluent also contained material with neuro-secretion inhibitory activity, which was resistant to heat treatment. Fractional assay of the TLC separated cardiac effluent demonstrated that the neurosecretion inhibitory activity chromatographed with PGE2 only.It has earlier been observed that endogenous PGs inhibit trans-mitter release in sympathetically stimulated organs. On the basis of the current data we suggest that PGE2 is the only physiological inhibitor of sympathetic transmitter release.  相似文献   

5.
We have investigated the effects of norepinephrine (NE) and acetylcholine (ACh) on prostaglandin (PGE2 and 6 keto-PGF) production by rabbit iris, measured by radioimmunoassay (RIA), and the type of phospholipase activated by NE in irides in which phosphatidylinositol (PI) was doubly prelabeled with [3H] myo-inositol and [1-14C] arachidonic acid (14C-AA), quantitated by radiometric and chromatographic methods. PGE2 output in 60 min (3.6 μg/g tissue) was 2.6 times greater than 6 keto-PGF. PG production is time-dependent and it is stimulated by NE and ACh in a dose-dependent manner. The Ne- and ACh-induced release of PGE2, measured by RIA, is mediated through α1-adrenergic and muscarinic cholinergic receptors, respectively, and it requeires Ca2+ for maximal stimulation. Studies on the mechanism of AA release PI in irides doubly prelabeled with 14C-AA and [3H] myo-inositol revelased the following: (a) Both Ne and ACh increased the breakdown of PI, and this was accompanied by a significant increase in the release of AA and consequently PGE2. The stimulatory effects of NE and ACh are mediated through α1-adrenergic and muscainic cholinergic receptors respectively. (b) The NE-induced formation of 3H-lyso PI and the NE-induced metabolism of 14C-1,2-diacyl-glycerol (DG) are time-dependent. Two pathways for AA release from PI are probably operaitve in the iris: (a) An indirect release by PI-specific phospholipase C which producers DG, followed by the actions of DG- and monoacylglycerol lipases on DG to release AA. (b) A direct release by phospholipase A2. Whether lyso PI is a product of the polypholipids such as prosphatidylcholine and phosphatidylethanolamine could also serve as a source for AA in PG synthesis. In conclusion, the data presented provide evidence that in the iris the neurotransmitter-stimulated release of PG and AA, from phosphoinositides, for PG synthesis is coupled to the activation of α1-adrenergic and muscarinic cholinergic receptors.  相似文献   

6.
Pretreatment of human lung fibroblasts with PGE2 but not PGF 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   

7.
To ascertain whether prostaglandins (PG) may play a role in the secretion of glucagon and in an attempt to elucidate the conflicting observations on the effects of PG on insulin release, the isolated intact rat pancreas was perfused with solutions containing 1.1 × 10−9 to 1.8 × 10−5M PGE2. In the presence of 5.6 mM glucose significant increments in portal venous effluent levels of glucagon and insulin were observed in response to minimal concentrations of 2.8 × 10−8 and 1.4 × 10−7M PGE2, respectively; a dose-response relationship was evident for both hormones at higher concentrations of PGE2. When administered over 60 seconds, 1.4 × 10−6M PGE2 resulted in a significant increase in glucagon levels within 24 seconds and in insulin within 48 seconds. Ten-minute perfusions of 1.4 × 10−6M PGE2 elicited biphasic release of both islet hormones; Phase I glucagon release preceded that of insulin. Both phases of the biphasic glucagon and insulin release which occurred in response to 15-minute perfusions of 10 mM arginine were augmented by PGE2. These observations indicate that PGE2 can evoke glucagon and insulin release at concentrations close to those observed by others in the extracts of rat pancreas. We conclude that PG may be involved in the regulation of secretion of glucagon and insulin and may mediate and/or modify the pancreatic islet hormone response to other secretagogues.  相似文献   

8.
The spontaneous output of prostaglandin (PG) I2 from the perfused mesenteric arterial bed in vitro was significantly higher in hypertensive rats than in normotensive rats. Sympathetic nerve stimulation (at 10Hz) of the mesenteric arterial bed from normotensive rats caused a rapid and short-lived (< 4 min) two-fold increase in PGI2 output and a smaller increase in PGE2 output. Sympathetic nerve stimulation (at 10Hz) of the mesenteric arterial bed from hypertensive rats failed to increase PGI2 and PGE2 output. It is not possible to conclude whether this lack of response is a cause or a result of hypertension. Surprisingly, norepinephrine administration stimulated PGI2 and PGE2 release from the mesenteric arterial bed of both normotensive and hypertensive rats. Obviously, differences exist in the responsiveness of rat mesenteric arteries to endogenous and exogenous norepinephrine concerning PG release between the normotensive and hypertensive states.  相似文献   

9.
The hypothesis that prostaglandins have a modulatory role in adrenergic neurotransmitter release was tested in the anesthetized dog. Inhibition of prostaglandin synthesis with indomethacin (10 mg/kg, i.v.) did not alter positive chronotropic responses to cardioaccelerator nerve stimulation or blood pressure responses to exogenous norepinephrine. In the presence of indomethacin, infusions of PGE2 (0.01 and 0.1 μg kg−1 min−1) also failed to influence the responses to cardioaccelerator nerve stimulation although the blood pressure responses to exogenous norepinephrine were reduced in a dose-related manner. It was concluded that endogenous prostaglandins and exogenous PGE2, the purported physiological inhibitor of neurotransmitter release in cardiac tissue, do not play a role in modulating chronotropic responses during cardioaccelerator nerve stimulation in the anesthetized dog.  相似文献   

10.
Prostaglandins (PG) of both the E and F series may serve as modulators of norepinephrine (NE) release from peripheral sympathetic neurons. We have studied the effects of PGE2 and PGF on the accumulation and release of 3H-NE in the CNS using synaptosomes isolated from rat hypothalami.The release of 3H-NE from synaptosomes superfused with Krebs-Ringer bicarbonate buffer was multiphasic with an initial fast release phase followed by a slower release. Raising KC1 concentration of the superfusion medium to 56mM during the slow release phase is known to stimulate 3H-NE release. PGE2 (1 × 10?6M) attenuated 3H-NE release during the fast phase and reduced the amount of 3H-NE released due to KC1 stimulation. At lower concentrations of PGE2 there was no change in the release profile. PGF was without effect on 3H-NE release at all concentrations tested.The accumulation of 3H-NE was significantly diminished by PGE2 at a concentration of 1 × 10?6M, while a lower concentration (1 × 10?7M) was ineffective. PGF had no effect on 3H-NE accumulation at all concentrations investigated.  相似文献   

11.
To ascertain whether prostaglandins (PG) may play a role in the secretion of glucagon and in an attempt to elucidate the conflicting observations on the effects of PG on insulin release, the isolated intact rat pancreas was perfused with solutions containing 1.1 × 10−9 to 1.8 × 10−5M PGE2. In the presence of 5.6 mM glucose significant increments in portal venous effluent levels of glucagon and insulin were observed in response to minimal concentrations of 2.8 × 10−8 and 1.4 × 10−7M PGE2, respectively; a dose-response relationship was evident for both hormones at higher concentrations of PGE2. When administered over 60 seconds, 1.4−10−6M PGE2 resulted in a significant increase in glucagon levels within 24 seconds and in insulin within 48 seconds. Ten-minute perfusions of 1.4 × 10−6M PGE2 elicited biphasic release of both islet hormones; Phase I glucagon release preceded that of insulin. Both phases of the biphasic glucagon and insulin release which occurred in response to 15-minute perfusions of 10 mM arginine were augmented by PGE2. These observations indicate that PGE2 can evoke glucagon and insulin release at concentrations close to those observed by others in the extracts of rat pancreas. We conclude that PG may be involved in the regulation of secretion of glucagon and insulin and may mediate and/or modify the pancreatic islet hormone response to other secretagogues.  相似文献   

12.
The effects of 6-keto-PGE1 on vascular resistance and vascular responses to sympathetic nerve stimulation and vasoconstrictor hormones were investigated in the feline mesenteric vascular bed. Infusions of 6-keto-PGE1 into the superior mesenteric artery dilated the mesenteric vascular bed and markedly inhibited vasoconstrictor responses to sympathetic nerve stimulation, norepinephrine and angiotensin II. The effects of 6-keto-PGE1 and PGE1 on vascular resistance and vasoconstrictor responses were quite similar and both substances inhibited responses to nerve stimulation and pressor hormones in a reversible manner. Responses to nerve stimulation, norepinephrine and angiotensin II were inhibited to a similar extent during infusion of 6-keto-PGE1 and PGE1. Results of these studies suggest that 6-keto-PGE1, a newly identified prostaglandin metabolite, and PGE1 possess the ability to inhibit the vasconstrictor effects of sympathetic nerve stimulation and pressor hormones by a nonspecific action on vascular smooth muscle in the feline small intestine.  相似文献   

13.
Prostaglandins (PG) of both the E and F series may serve as modulators of norepinephrine (NE) release from peripheral sympathetic neurons. We have studied the effects of PGE2 and PGF on the accumulation and release of 3H-NE in the CNS using synaptosomes isolated from rat hypothalami.The release of 3H-NE from synaptosomes superfused with Krebs-Ringer bicarbonate buffer was multiphasic with an initial fast release phase followed by a slower release. Raising KC1 concentration of the superfusion medium to 56mM during the slow release phase is known to stimulate 3H-NE release. PGE2 (1 × 10−6M) attenuated 3H-NE release during the fast phase and reduced the amount of 3H-NE released due to KC1 stimulation. At lower concentrations of PGE2 there was no change in the release profile. PGF was without effect on 3H-NE release at all concentrations tested.The accumulation of 3H-NE was significantly diminished by PGE2 at a concentration of 1 × 10−6M, while a lower concentration (1 × 10−7M) was ineffective. PGF had no effect on 3H-NE accumulation at all concentrations investigated.  相似文献   

14.
The effect of cAMP on prostaglandin production may depend on cell types. To clarify the relationship between PG and cAMP, we examined arachidonate's effects on PG synthesis and intracellular cAMP accumulation in monolayers of rat gastric mucosal cells. These cells produced PGE2, PGI2 and thromboxaneA2 (TXA2) in amounts of 316±18, 100±7 and 30±5 pg per 105 cells in 10 min, respectively, in response to 10μM arachidonic acid (AA). The production of these PG, however, leveled off subsequently. Cells initially exposed to AA responded poorly to a subsequent stimulation by AA. AA simultaneously stimulated intracellular cAMP accumulation; this stimulatory effect on cAMP production was abolished by the pretreatment with indomethacin. Nevertheless, the pretreatments with dibutyryl cAMP (0.1–5mM) did not alter the amount of subsequent AA-induced PGE2 production. Furthermore, the preincubation with 1mM isobutyl methyl xanthine also failed to affect PGE2 synthesis, while it increased intracellular cAMP accumulation. Our studies suggest (1) AA stimulates intracellular cAMP formation in cultured gastric mucosal cells, linked with conversion of AA to cyclooxygenase metabolites, (2) AA-induced PG production is limited in these cells, and (3) it seems, however, unlikely that intracellular cAMP modulates AA metabolism to PG.  相似文献   

15.
The effect of estradiol and tamoxifen on prostaglandin (PG) synthesis by rabbit articular chondrocytes in secondary monolayer cultures was investigated. Radioimmunoassay for PGE2, PGF, 6-oxo-PGF and thromboxane B2 was performed on media from cultures containing estradiol and tamoxifen (10−12M-10−7-M). Radiometric thin-layer chromatography was also carried out. The time course of estradiol/tamoxifen effect on chondrocyte PG synthesis was evaluated and its relationship to cell density in culture examined. Estradiol stimulated the synthesis of PGs by chondrocytes. Stimulation was noted at picomolar concentrations of estradiol without further stimulation at markedly higher concentrations. In time studies, after a lag, the effect of estradiol was present fully by 5 hrs, remained steady for 24 hrs and then declined by 48 hrs. Estradiol stimulation of PG synthesis was dependent upon chondrocyte culture plating density. Tamoxifen stimulated chondrocyte PG synthesis to relatively lower levels than estradiol. The characteristics of estradiol/tamoxifen stimulation of chondrocyte PG synthesis suggest a mechanism involving estradiol cytoplasmic receptors.  相似文献   

16.
The effects of oestradiol, oxytocin, progesterone and hydrocortisone on prostaglandin (PG) output from guinea-pig endomerium, removed on days 7 and 15 of the oestrous cycle and maintained in tissue culture for 3 days, have been investigated. Oetradiol (3.7 to 3700nM) and oxytocin ( 2 to 200pM) did not stimulate endometrial PGF output, thus not confirming the findings of a previous report (Leaver & Seawright, 1928), nor did they stimulate the outputs of PGE2 and 6-keto-PGF. In fact, oestradiol (3700nM) inhibited the outputs of PGF, PGE2 and, to a lesser extent, 6-keto-PGF. Progesterone (3.2 to 3200nM) inhibited the outputsof PGF and PGE2; hydrocortisone (2.8 to 2800nM) had no effect on endometrial PG output. These findings indicate that the inhibitory effect of progesterone on endometrial PG synthesis and release in the guinea-pig is not due to progesterone having a glucocorticoid-like action. Furthermore, progesterone had no effect on 6-keto-PGF output, suggesting that the mechanisms controlling endometrial PGI2 synthesis (as reflected by measuring 6-keto-PGF) are different from those controlling endometrial PGF and PGE2 synthesis.  相似文献   

17.
Prostaglandin (PG) E2 was the major PG released from the superfused guinea-pig uterus on Day 7, followed by in descending order 6-oxo-PGF, thromboxane (TX) B2 and PGF. However, the outputs of all four substances were low and were very similar. By Day 15, PGF output from the superfused uterus had increased 21.9-fold, whereas the outputs of PGE2, 6-oxo-PGF and TXB2 had increased only 1.8-, 2.9- and 1.2-fold, respectively. A mechanism is apparently “switched on” between Days 7 and 15 which causes a fairly specific increase in the release of PGF from the uterus.Progesterone and/or estradiol had no effect on PG or TX release when superfused over the uterus on Day 7, nor did they have any effect on PG and TX release from the Day 15 uterus when administered separately. When administered together, however, they significantly inhibited PGF, PGE2 and 6-oxo-PGF, but not TXB2, release from the Day 15 uterus. Oxytocin had no effect on PG release from the Day 7 or Day 15 uterus, while A23187 stimulated PGF, 6-oxo-PGF and, to a lesser extent, PGE2 release from the uterus on both Days 7 and 15 Oxytocin is apparently not important for stimulating PGF release from the guinea-pig uterus in relation to luteolysis, whereas increasing intracellular free Ca++ levels may be part of the mechanism for “switching on” uterine PG synthesis. Furthermore, changes in intracellular free Ca++ levels in the endometrium may be responsible for the pulsatile nature of PGF release from the uterus.  相似文献   

18.
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 PGF. On the other hand, cimetidine (10−5M) enhanced the basal release of PGE2 but had no action on the outputs of PGs E1 or F. The enhancing effect of H on the production and release of PGF 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 PGF 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-PGF 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 PGF, apparently via the activation of H2-receptors, enhancing adenylate-cyclase. These effects appear to increase uterine 9-keto-reductase activity which transforms PGE2 into PGF. Relationships between the foregoing results and those evoked by estradiol, are also discussed.  相似文献   

19.
The effect of various factors upon prostaglandin (PG) production by the osteoblast was examined using osteoblast-rich populations of cells prepared from newborn rat calvaria. Bradykinin and serum, and to a lesser extent, thrombin, were also shown to stimulate PGE2 and 6-keto-PGF (the hydration product of PGI2) secretion by the osteoblastic cells. Several inhibitors of prostanoid synthesis, dexamethasone, indomethacin, dazoxiben and nafazatrom, were tested for their effects on the calvarial cells. All inhibited PGE2 and PGI2 (the major arachidonic acid metabolites of these cells) production with half-maximal inhibition by all four substances occuring at approximately 10−7 M. For dazoxiben and nafazatrom, this was in contrast to published results from experiments which have indicated that the compounds stimulated PGI2 production. Finally, since the osteoblasts is responsive to bone-resorbing hormones, these were tested. Only epidermal growth factor (EGF) was shown to modify PG production. At early time EGF stimulated PGE2 release, however, the predominant effect of the growth factor was an inhibition of both PGE2 and PGI2 production by the osteoblastic cells. The present results suggest that the bone-resorbing hormones do not act to cause an increase in PG by the esteoblast and that any increase in PG production by these cells may be in response to vascular agents  相似文献   

20.
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   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号