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)

In a previous investigation of children infected with pertussis during the first week of paroxysmal stage, we found a 50-75% reduction of the isoprenaline (IPN)-induced cAMP response in peripheral MN leucocytes. In order to characterize these findings further, intact human MN leucocytes from healthy adults were treated with PT in vitro. Basal, as well as prostaglandin E1-stimulated cAMP levels were decreased by PT in a dose-dependent fashion over a range of 0.01 to 1000 ng ml-1 to about 65% of control levels. Stimulation of PT-pretreated cells (100 ng ml-1, 90 min, 37 degrees C) showed significantly reduced IPN and PGE1-induced cAMP accumulation, indicated by a depression and shift of the dose-response curves to the right. In contrast, cAMP generation was unchanged by forskolin, a diterpene that is believed to directly stimulate adenylyl cyclase. The anti-allergic drug ketotifen had no direct effects on basal, IPN or PGE1-induced cAMP responses; however the inhibitory actions of PT pretreatment on cAMP levels were diminished (basal and isoprenaline-stimulated) or reversed (PGE1-stimulated). To further locate the site of impaired cAMP responses, beta-adrenoceptor binding, as well as displacement characteristics of the receptor, were estimated by 125I-cyanopindolol binding to a plasma membrane fraction pretreated with or without PT. No differences in beta-adrenoceptor number or in the affinities of the binding sites could be detected. These data are in close agreement with the findings on MN leucocytes from pertussis-infected children and support the notion of PT-induced impaired signal transduction in the cAMP generating system in human MN leucocytes.
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PMID:Inhibitory effects of pertussis toxin on the cAMP generating system in human mononuclear leucocytes. 216 75

Patients (n = 23) with definite or classical rheumatoid arthritis were given 18 g/day fish oil in gelatin capsules which provided 3.2 g/day EPA and 2.0 g/day DHA. The treatment period was 12 weeks followed by a 4 week washout period. Fish oil supplementation to the diet resulted in a substantial increase in the content of EPA and DHA in each of the plasma fractions examined (PL, TG, and CE). Little change was seen in the AA level of the TG and CE fractions but a modest decrease in AA was seen in PL. However the intake of fish oil caused a significant depression in the content of DGLA in the PL (p less than 0.005) and CE (p less than 0.01) fractions relative to baseline values. All changes had reverted to near baseline levels 4 weeks after dietary intervention. Since DGLA is the precursor of PGE1, which has been shown to be anti-inflammatory, our findings suggest that the anti-inflammatory effects of fish oil consumption could be mitigated by an associated reduction in DGLA.
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PMID:The effect of dietary fish oil supplement upon the content of dihomo-gammalinolenic acid in human plasma phospholipids. 216 63

Endogenous proliferation of corneal epithelial cells is regulated by a bidirectional control process characterized by an adrenergic, cAMP-dependent 'off', and a cholinergic, muscarinic cGMP-dependent 'on' response. The adrenergic receptor(s) are located in the plasma membrane (microsomal fraction), whereas the novel feature of the system is a cholinergic receptor specific for acetylcholine (ACH) located in the nuclear membrane. Exogenous substances which raise intracellular cAMP levels such as isoproterenol or PGE1, shut off epithelial mitosis: and, carbamylcholine or ACH raise intranuclear cGMP levels and increase mitosis by specific, regulatory stimulation of RNA-polymerase II activity. We believe that this regulatory system explains the transitory mitotic suppression induced by superficial corneal wounding (interruption of adrenergic fibres, chalone-effect); and the marked, permanent depression of epithelial mitosis associated with decreased intracellular ACH levels which are produced by total corneal denervation, and which results in neurotrophic keratitis.
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PMID:The molecular basis of neurotrophic keratitis. 255 41

Platelet alpha 2-adrenergic receptor binding and prostaglandin responsivity were measured in depressed patients. Depressed patients had significantly higher platelet 3H-dihydroergocryptine (3H-DHE) binding values than controls. Depressed patients also showed significantly reduced prostaglandin E1-stimulated cyclic adenosine 3',5'-monophosphate (cAMP) production and significantly decreased % inhibition of cAMP production by norepinephrine. These results support the suggestion that there may be a dissociation between alpha 2-adrenergic receptor binding and responsivity in depression. There were no significant correlations between platelet adrenergic variables and other indices of noradrenergic function. However, there was a significant correlation between 3H-DHE binding values and basal plasma levels of cortisol.
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PMID:Platelet adrenoceptors and prostaglandin responses in depressed patients. 255 22

A 14-year-old girl was admitted with chief complaints of edema and chest pain. She had hepatomegaly, but did not have heart murmur and accentuation of the pulmonary component of the second heart sound. The electrocardiogram showed right axis deviation, negative T wave in V3,4 and ST depression in III, aVF. But right ventricular hypertrophy was not dominant. Chest radiography showed a cardiothoracic ratio of 54% and a slight prominence of proximal pulmonary arteries. The edema was soon diminished only by the diuretics, but it appeared again without the diuretics. At the cardiac catheterization 3 months after the onset of symptoms, the pulmonary arterial pressure was 150/85 mmHg and the pulmonary resistance was 3,232 dyn/sec/cm5. The right atrial pressure was 9.5 mmHg and oxygen saturation at the pulmonary artery was 31.0%. Prostaglandin E1 reduced the pulmonary artery pressure only a little, but raised the systemic pressure. The patient was treated with several vasodilators, but her condition deteriorated rapidly and she developed severe right ventricular failure. She died only 8 months after the onset of symptoms and 5 months after the catheterization. At autopsy, histological examination demonstrated intimal fibrotic thickening of the small-sized pulmonary arteries and organizing thrombus. But there was not plexiform lesion. Heart failure was easily improved when she was first admitted. But after 3 months the cardiac catheterization revealed that her condition was already severe. Several vasodilators was not effective to such a rapidly progressive primary pulmonary hypertension.
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PMID:[A case of rapidly progressive pulmonary pulmonary hypertension in a 14-year-old girl]. 259 31

The inhibitory effects of norepinephrine (NE) on the cyclic adenosine-3',5'-monophosphate (cAMP) response to prostaglandin E1 (PGE1), a measure of alpha 2-adrenergic receptor function, have been compared in platelets from drug-free schizophrenic patients, depressive patients, and normal controls. The absolute value of the inhibition by NE of the cAMP response to PGE1 was smaller in platelets from schizophrenic and depressive patients than in controls. However, this result was secondary to the smaller baseline platelet cAMP response to PGE1 in patients with these disorders. Effects of NE on cAMP production did not discriminate between actively ill and remitted patients with either schizophrenia or depression. Platelet alpha 2-receptor sensitivity, as measured by the effects of NE on cAMP production, does not appear to be altered in these psychiatric disorders.
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PMID:Platelet alpha 2-adrenergic receptor function in psychiatric disorders. 283 62

The rat uterus generates and releases prostaglandins (PGs) of the series 2 as well as PGs of the series 1. The main purposes of the present study are to compare the effects of norepinephrine (NE) on the production and outputs of PGE1, PGE2 and PGF2 alpha by the uterus isolated from ovariectomized rats, treated or not with 17-beta-estradiol and to explore also, whether the effects of NE on PG synthesis are mediated through alpha, beta or both types of adrenoreceptors. Segments of control uterine horns obtained from ovariectomized rats generated and released into the incubating solution, equal amounts of PGE1, PGE2 and PGF2 alpha and propranolol (10(-6) M) or phentolamine (10(-6) M) failed to alter this basal production of PGs. Norepinephrine (3 X 10(-6) M) significantly depressed the outputs of PGE1 and PGF2 alpha but enhanced, also significantly, the release of PGE2. In the presence of the beta-adrenoreceptor blocker, propranolol, the reduction induced by NE on the output of PGE1 was not altered, but the stimulatory influence of NE on the release of PGE2 as well as the depression on the output of PGF2 alpha, were abolished. On the other hand the diminution evoked by NE on the release of PGF1 and PGF2 alpha as well as the increment induced on PGE2 output, were inhibited by the presence of phentolamine in the incubating solution. Uterine horns from ovariectomized rats treated with 17-beta-estradiol released into the incubating solution significantly more PGF2 alpha than PGE1 or PGE2. NE, either alone of in the presence of alpha 0 or beta-adrenoceptor blockers, did not modify this pattern of PG production. A possible mechanism(s) of action for NE on PG synthesis is discussed.
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PMID:Norepinephrine alters PGE2/PGE1 output ratio in isolated uterus from ovariectomized rats. 287 85

Six point concentration-response curves were established for the contractile effect of prostaglandin E2 (PGE2) on helically-cut strips of human chorionic plate arteries. Tissues were then allocated to one of four treatment groups: a control group and 3 groups exposed to the calcium channel blocker nitrendipine at 10(-9), 10(-7) or 10(-5) M. The concentration-response curves were then repeated. The addition of nitrendipine was associated with a significant depression of the induced contraction. The contractile response to the lower doses of PGE2 was replaced by a small relaxation in 63% of the treated tissues. It is suggested that in these tissues PGE2 exerts its constrictor effect via the receptor-operated channels and that nitrendipine is blocking this effect. Similar experiments performed with PGE1 showed great variability in the initial response. Nitrendipine 10(-5) M failed to exert any detectable effect on this response. Pregnancy-induced hypertension is associated with vasoconstriction in both the maternal and placental circulations. There also appears to be a relative excess of vasoconstrictor eicosanoid production. Nitrendipine may be of use in the treatment of this condition.
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PMID:The effect of a calcium antagonist, nitrendipine, on the responses of isolated strips of human, chorionic plate artery to prostaglandins E2 and E1. 293 11

Plasma prostaglandin E1 and E2, and quantitative and qualitative measures of immune function, were determined in depressed patients and healthy controls. Prostaglandin E2 was significantly elevated in the depressed group, and prostaglandin E1 showed a trend in the same direction. Lymphocyte stimulation responses, as measured by phytohemagglutinin, concanavalin A, and pokeweed mitogen, were significantly lower in the depressed group. Helper and suppressor T cell percentages did not significantly differ in the two populations. In the depressed group, prostaglandin E1 showed a significant inverse correlation with concanavalin A, and prostaglandin E2 showed a similar trend. These preliminary data suggest prostaglandins of the E series may be related to abnormalities of cellular immunity previously documented in depression.
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PMID:Depression, immunocompetence, and prostaglandins of the E series. 293 97

The present study was performed in order to evaluate whether norepinephrine (NE) can modulate the synthesis and release of 1 and 2 series of prostaglandins (PGs) by the isthmic region of preovulatory sow oviducts and also to clarify whether the action of the neurotransmitter is mediated through alpha, through beta or through both types of tissue adrenoreceptors. NE, at a concentration of 1 microgram/ml, depressed significantly (P less than 0.05) the basal output of PGE1 and enhanced (P less than 0.01) the release of PGE2 but, did not modify, the output of "PGF2 alpha-like material". Propranolol (10(-7)M) failed to alter the basal output of "PGE1, PGE2 or PGF2 alpha-like material". In the presence of this beta-adrenoreceptor blocker, the depression induced by NE on PGE1 output, was abolished; its stimulatory influence on the release of PGE2, was eliminated and no effect was detected regarding PGF2 alpha. On the other hand, phentolamine (10(-6)M) did not alter the basal output of "PGE1, PGE2 or PGF2 alpha-like material" and also failed to modify the depression induced by NE on PGE1 release. However, this alpha adrenoceptor blocker completely inhibited the stimulatory action of NE on the output of PGE2 into the incubating medium. The foregoing results document opposite actions of NE on PGE1 and PGE2 outputs from the isthmic region of proestrous sow oviducts and suggest the involvement of beta-adrenoreceptors in both disparate influences. The activation of alpha adrenoreceptors also appears associated with the enhancing effect of the agonist on the release of PGE2. The possible physiological significance of these findings is discussed in terms of the function of the isthmic region as an "adrenergic sphincter" able to influence ovum transport around the moment of ovulation.
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PMID:On the synthesis of prostaglandins E1, E2 and E2 alpha by sow oviducts. Differential modulation of 1 and 2 series of prostaglandins by norepinephrine. 298 54


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