Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study examines the possible role of endogenous prostaglandins (indomethacin; PGF2a; PGE1; PGE2; and prostacyclin or PGI2) on the spontaneous motility of the human ampullar and isthmus deprived of the mesosalpinx. Fallopian tubes were obtained from 12 patients who had hysterectomy and salpingo-oophorectomy. The segments of the tubes were prepared for contractile recordings as previously described and divided into 2 groups: 1) ampullar and isthmic segments were followed by spontaneous variations in motility during 30 minutes; and 2) cumulative close-response curves for PGI2 were constructed for ampullar and isthmic segments 30 minutes after the end of equilibrium. Contractile functions were evaluated in terms of amplitude of isometric developed tension (IDT) and frequency of contraction, and when pertinent, changes in resting basal tone. Student's t-test was used for statistical analysis, and differences between means were considered significantly at P=0.05 or less. Indomethacin significantly enhance the IDT of the isthmic but not the ampullar region. However, a single and identical concentration of 10-6M of PGE1 and PGI2 depressed the ampullar while PGE2 and PGF2a enhanced its contractions. In the isthmus, PGE1, PGE2 and PGF2a augmented while PGI2 diminished the IDI. Both ampullar and isthmic regions exhibited a dose-dependent depression of IDI and contractile frequency. In the isthmus, PGI2 produced a biphasic action on resting basal tone while in the ampulla, only a progressive dose-dependent decline was seen. Prostacyclin may be synthesized by the isthmic region of the human fallopian tubes, but whether it occurs in vivo or what its physiological significance is remains to be seen.
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PMID:Spontaneous motility of isolated mesosalpinx-free isthmic and ampullar segments from human oviducts, and the influences of indomethacin and prostacyclin (PGI2). 4 1

Pressure increases elicited by contractions of the circular muscle of the isolated guinea-pig vas deferens in response to nerve stimulation were recorded. In contrast to longitudinal muscle which contracted in response to 1--50 pulses, circular muscle responded only to longer trains of pulses (10--500) at a frequency of 10 Hz. Atropine (1.4 muM) caused a slight depression of responses to 100 shocks. Phentolamine at a concentration of 2.6 muM failed to inhibit the response to stimulation, but a higher concentration (53 muM) caused a definite blockade. Guanethidine (25 muM) strongly reduced the responses. With a stimulus train of 100 pulses no inhibition by prostaglandin E1 (PGE1) (0.028 muM) could be demonstrated; however, at a lower number of shocks (20--50) a clearcut depression was observed. The lower the number of pulses the more marked was the depression. The observation that PGE1 failed to block the contractions evoked by noradrenaline (59 muM) suggests a presynaptic inhibitory action of the prostaglandin. It is suggested that noradrenaline is the transmitter in both muscle coats of the guinea-pig vas deferens and that the neuroeffector junctions are sensitive to the effect of PGE1.
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PMID:Inhibition of neuromuscular transmission by prostaglandin E1 in the circular muscle of the guinea-pig vas deferens. 18 81

Ticlopidine, when orally administered to rats, resulted in activation of basal and prostaglandin E1 (PGE1)-stimulated adenylate cylase activity through increase in affinity of the cyclase in platelet membrane to PGE1, although it failed to affect adenosine- or sodium fluoride-stimulated activity of the enzyme. In washed platelets, Ticlopidine also activated basal and PGE1-stimulated activity of the cyclase and prevented reduction in the cyclase activity caused by low concentrations of PGE2. Furthermore, Ticlopidine inhibited malondialdehyde formation in platelets induced by thrombin but failed to inhibit that caused by exogenous arachidonic acid. Adenosine 3',5'-cyclic monophosphate (c-AMP): phosphodiesterase activity of platelet lysate was not significantly affected by Ticlopidine treatment. These findings indicate that Ticlopidine inhibits platelet aggregation and prostaglandin synthesis from endogenous substrate through activating basal and PGE1-stimulated activity of the cyclase, preventing PGE2-induced depression of the cyclase activity and thus increasing platelet c-AMP level.
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PMID:Mode of action of ticlopidine in inhibition of platelet aggregation in the rat. 22 22

5-Hydroxytryptamine (5-HT) and epinephrine were applied by microiontophoresis to single neurons in the isolated spinal cord of the frog. 5-HT depressed all but two of the responsive cells, whereas the response to epinephrine consisted exclusively of depression. 5-HT action was more marked than that of epinephrine on most cells. With either compound, responseve units were diffusely distributed throughout the tissue. While it was proven that prostaglandin E1 (PGE1) exerts a direct excitatory action on spinal neurons, no evidence of an antagonism between PGE1 and the monoamines was obtained. These findings provide additional support to the hypothesis that 5-HT and epinephrine are transmitters in the frog spinal cord. The possibility that PGE1 may 'modulate' the responsiveness of spinal neurons to the monoamines was not confirmed.
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PMID:Microiontophoresis of 5-hydroxytryptamine, epinephrine, and prostaglandin E1 on spinal neurons in the frog. 30 25

Sensitivity of neurones in the rostral hypothalamus of methoxyflurane anesthetized cats to the prostaglandin synthetase inhibitors (PGSIs), salicylate and fenoprofen, has been examined using the technique of microiontophoresis. Results were compared with sensitivity to prostaglandin (PG) E1 and no noradrenaline (NA) and 5-hydroxytryptamine (5HT). Simultaneous applications of PGSIs and NA or 5HT were made to investigate the role of PG in monoamine induced changes in neuronal excitability. PGSIs did not excite these cells, but depression were common, particularly with fenoprofen. PGE1 did not reverse the depressions. NA and 5HT responses were generally unaffected by simultaneous PGSI application and responsiveness to PGSIs was found to be unrelated to amine sensitivity. The results support the conclusion that PGSIs have a depressant action on neurones in this region, which may not be related to inhibition of prostagladin synthesis, and that the actions of microiontophoretically applied NA and 5HT are not dependent upon PG.
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PMID:Action of prostaglandin synthetase inhibitors on rostral hypothalamic neurones: thermoregulation and biogenic amines. 81 16

In male Wistar rats PGF2alpha or PGE1 were injected intracerebroventricularly (icv) in a dose of 1 or 10 mug. Immediately or 1 hr after injection the locomotor and exploratory activity were measured. The levels of noradrenaline (NA), dopamine (DA) 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA) and acetylcholine (Ach) were measured in discrete brain areas. Both PGs applied ivc caused the depression of locomotor and exploratory activity in rats. PGE1 acted longer. Both substances but PGE1 more intensively affected the level of estimated biogenic amines in different brain structures. It is concluded that PGF2alpha and E1 are central nervous depressants. Both PGs affect neurons producing NA or 5-HT or Ach in discrete areas of brain in different manner. There is different susceptibility of brain structures on PGs action.
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PMID:Central effects of prostaglandins F2alpha and E1. 101 72

Adenosine diphosphate (ADP) stimulates the synthesis of prostaglandin E1 (PGE1) in lysed platelets from normal subjects, patients with affective illness but not in platelets from cases of schizophrenia. The stimulation is concentration-dependent and follows a curve which is mildly sigmoid in the normal, markedly sigmoid in depression and hyperbolic in mania.
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PMID:Effect of ADP on PGE1 formation in blood platelets from patients with depression, mania and schizophrenia. 120 54

Rabbit abdominal aorta was irradiated with single or repeated doses up to 10 Gy. The rabbits were killed at different time intervals after irradiation. 5 micrograms/kg x 6/hr PGE1 or its biologically active metabolite 13,14-DH-PGE1 were administered either 6 hours before or 6 hours after irradiation. The administration of both PGEs reduced radiation-induced mitotic activity (3H-thymidine incorporation) and extracellular matrix [collagen-(14C-proline) and glycosaminoglycan (35-S-sulphate)]-formation as determined by means of autoradiography. The initial peak increase in vascular PGI2-synthesis was partly abolished, while the long lasting depression was less pronounced. 13,14-DH-PGE1 was only slightly less active as compared to the parent compound. Pre-radiation treatment was more effective than post-irradiation therapy. These findings suggest that both the PGs exert significant radiation-protective actions on the arterial wall.
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PMID:Prostaglandin (PG) E1 and 13,14-dihydro (DH) PGE1 are diminishing radiation-induced arterial damage. 163 12

Since the sepsis syndrome is associated with depressed vascular reactivity, it may be incorrect to assume that pharmacologically mediated changes in cardiac output will be proportionately distributed at the regional level of the circulation. We examined the effect of hyperdynamic sepsis and the concurrent administration of the vasodilatory prostaglandin (PGE1) on the regional distribution of blood flows (Q) in unanesthetized sheep rendered septic by cecal ligation and perforation. Systemic Q progressively increased throughout a 48-h study period after cecal ligation and perforation. Simultaneously, organ Q, measured by the radioactive microsphere technique, was depressed to the pancreas, but increased to the heart, gallbladder, brain, and colon; the increased Q to both heart and gallbladder was greater than the simultaneous increase in systemic Q in this septic study. With the infusion of PGE1 (1 microgram/kg/min), mean arterial perfusing pressures fell, while the cardiac index increased further over that recorded during the 48-h septic study. Despite this depression in arterial pressures, the only significant effect of PGE1 on the interorgan distribution of Q was in the renal circulation, where it was demonstrated that kidney Q fell. We conclude that (1) hyperdynamic and normotensive sepsis exerted nonhomogeneous effects on the distribution of organ Q, and (2) an increased systemic Q during PGE1 infusion was proportionately distributed to all organs, except the kidneys, where Q paradoxically fell. The latter finding suggests that the regulation of kidney Q may be depressed across the normal range of arterial perfusing pressures in the sepsis syndrome. Further investigation is essential to understand the effect of clinical interventions on the control of tissue O2 flux at both the regional and microregional levels of the circulation.
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PMID:Effect of PGE1 on altered distribution of regional blood flows in hyperdynamic sepsis. 195 17

The effects of prostaglandin F2 alpha, prostaglandin E1, prostaglandin E2 and the thromboxane A2 analogue U46619 were determined in ring segments of human hand veins. All prostanoids except prostaglandin E1 elicited contraction. The order of potency was U46619 greater than prostaglandin F2 alpha greater than prostaglandin E2. The thromboxane receptor antagonists BM13,505 and AH23848 both caused a parallel rightward displacement of the concentration-response curve for U46619 without depression of the maximum contraction, suggesting competitive antagonism. Schild plots for both antagonists yielded regression lines with slope indices not significantly different from unity. The pA2 values for BM13,505 and AH23848 were 7.9 and 8.4 respectively. Both antagonists also effectively inhibited prostaglandin F2 alpha-induced contractions. However, AH23848 significantly reduced the maximum response, and the results with BM13,505 gave no clear indication of the type of inhibition. In vein segments submaximally contracted by 5-hydroxytryptamine, prostaglandins E1 and E2 produced a biphasic response with a relaxation at low and a contraction at high concentrations. Prostaglandin F2 alpha and U46619 failed to elicit relaxation under these conditions. However, in the presence of either thromboxane receptor antagonist, prostaglandin F2 alpha but not U46619 produced a relaxation. The results are compatible with the presence of at least two prostanoid receptors in human hand veins, a contraction-mediating thromboxane receptor and an as yet unclassified receptor eliciting relaxation. U46619 was a potent agonist at the thromboxane receptor and prostaglandin E1 and E2 preferentially stimulated the relaxation-mediating receptor, whereas prostaglandin F2 alpha appeared to be active at both receptor sites.
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PMID:Characterization of contraction-mediating prostanoid receptors in human hand veins: effects of the thromboxane receptor antagonists BM13,505 and AH23848. 205 48


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