UMLS:C0011570 - FACTA Search

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ontogenetic renal responsiveness to exogenous cortisol was examined in the chronically cannulated ovine fetus. The contribution of effects at proximal and distal tubule of the kidney were studied also. Cortisol (81.5 micrograms/h) was infused into immature ovine fetuses (mean gestational age -113.9 days) on five occasions and increased blood cortisol from 0.8 +/- 0.5 to 21.3 +/- 6.2 nmol/liter. This dose of cortisol produced a highly significant diuresis and natriuresis, in part due to an increase in GFR and in part due to a significant decrease in proximal tubular reabsorption of sodium. Cortisol (107.2 +/- 4.7 micrograms/h) was infused into mature fetuses (mean gestational age 133.4 days) and produced an increase in blood cortisol concentration from 11.4 +/- 5.6 to 33.7 +/- 6.8 nmol/liter. No natriuresis or diuresis was seen in the mature fetuses. Cortisol caused a significant depression of proximal tubular sodium reabsorption in mature fetuses, but this extra load was reabsorbed in the distal tubule in these fetuses. The inability of the premature or very low birth wt baby to maintain normal sodium balance on a standard salt intake may be due, at least in part, to a "fetal" renal response to the high plasma cortisol concentrations found in such babies. As the kidney matures it becomes capable of increasing distal tubular sodium reabsorption to compensate for any increased distal tubular fluid delivery.
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PMID:Gestational changes in renal responsiveness to cortisol in the ovine fetus. 277 10

The present study has investigated the question of whether or not hydrocortisone as a gene regulator plays a role in the expression of carcinogenic and cocarcinogenic actions of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and NaCl at the gastric epithelium. The interaction of local hydrocortisone, MNNG and NaCl was studied in vitro and in vivo using Swiss/ICR mice of both sexes. MNNG inhibited specific hydrocortisone binding with the cytoplasmic receptor from the glandular stomach of mouse. The intake of both excess NaCl and MNNG induced an increase in hydrocortisone turnover in the glandular stomach of mouse. Likewise, administration of either excess NaCl or MNNG increased the activity of ornithine decarboxylase in the glandular stomach of mouse. Long-term use of a salt-rich diet and MNNG drink induced an irreversible reduction in water consumption without affecting NaCl consumption, a dissociation of the hydrocortisone effect. The aforementioned MNNG effect on water turnover was more marked in female than in male mice. It is suggested that NaCl and MNNG produce a state of corticosteroid stimulation and androgen depression at the glandular stomach epithelium of mouse--a reproduction of the hormonal markers of gastric cancer.
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PMID:Interaction between N-methyl-N'-nitro-N-nitrosoguanidine and 2 steroid hormones in the glandular stomach of mouse. I. Acceleration of hydrocortisone turnover by use of a salt-rich diet and the carcinogen. 277 56

We have determined zeta-potentials for dimyristoylphosphatidylcholine (DMPC) and dipalmitoylphosphatidylcholine (DPPC) membranes by measuring the electrophoretic mobility of multilayered vesicles and the temperatures of the gel-to-ripple-to-fluid phase transitions of sonicated vesicles by a photometric method. Some conclusions are: (1) The zeta-potentials of DMPC and DPPC vesicles become negative due to adsorption of ionized pentachlorophenol (PCP), (2) their magnitude changes, step-like, on gel-to-fluid transition and (3) the temperature of the step-like change in zeta-potential decreases with an increase in PCP concentration. (4) PCP exhibits a large effect on membrane structure: It induces an isothermal phase change from the ordered to disordered state, which is enhanced by monovalent salt in the aqueous phase. (5) Both ionized and unionized PCP decrease the melting phase transition temperature and abolish the pretransition, (6) the unionized species increases the melting transition width and (7) the ionized species is more potent in abolishing the pretransition. (8) The shorter chain lipid (DMPC) is more sensitive to the presence of PCP; the maximum decrease in delta Tt is 13 K (DMPC) and 7 K (DPPC) in the presence of ionized PCP. We have shown experimentally, by comparing the delta Tt from photometric studies with the density of adsorbed PCP derived from zeta-potential isotherms, that (9) the shift of the melting phase transition temperature increases linearly with the density of adsorbed PCP. (10) In contrast to membranes made of negatively charged lipids, the transition temperature of DMPC and DPPC membranes in the presence of PCP further decreases in the presence of monovalent salt. The salt effect is due to screening of the membrane surface leading to enhanced adsorption of ionized PCP and a depression in transition temperature. (11) It is shown that both the adsorption and the changes of gel-to-fluid phase transition temperature can be described in terms of the Langmuir-Stern-Grahame model and (12) proposed that future studies of membrane toxicity of PCP should be focused on its pH dependence.
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PMID:Pentachlorophenol-induced change of zeta-potential and gel-to-fluid transition temperature in model lecithin membranes. 277 33

Locus coeruleus may have a function in central blood pressure regulation and possibly in the pathogenesis of hypertension. In keeping with this notion, we have recently shown that deoxycorticosterone acetate (DOCA)-salt hypertensive rats demonstrate a greater increase in blood pressure induced by locus coeruleus stimulation than control animals. In an attempt to elucidate the underlying mechanisms leading to this alteration in responsiveness of the locus coeruleus, the sensitivity of noradrenergic neurons of the locus coeruleus to the transmitter candidates, epinephrine and glutamate, was investigated in DOCA-prehypertensive (3 days post-DOCA), DOCA chronic hypertensive (6-8 weeks post-DOCA) and control rats using conventional microiontophoretic and single cell recording techniques. Iontophoretically applied epinephrine produced a current-dependent decrease in spontaneous firing rate of all noradrenergic neurons in both DOCA-treated and control rats. Locus coeruleus neurons of DOCA-treated rats at 3 days and 6-8 weeks were less sensitive to epinephrine than those of control rats and the magnitude of the depression in spontaneous firing rate was less. By contrast, iontophoretic applications of glutamate produced an increase in activity of all noradrenergic locus coeruleus neurons. However, there was minimal difference in glutamate sensitivity between neurons of DOCA and control rats. Since the changes in epinephrine sensitivity are apparent not only in the chronic stage but also in the prehypertensive stage, our findings suggest a potential role of the adrenergic input to the locus coeruleus in the pathogenesis of DOCA-hypertension.
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PMID:Alterations in responsiveness of noradrenergic neurons of the locus coeruleus in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. 288 Jun 43

We isolated simian virus 40 (SV40) chromosomes from lytically infected CV-1 cells at various times during the late phase and transcribed them in vitro with either whole-cell or nuclear extracts of HeLa cells. The late promoter was 3- to 10-fold more active than the early promoter. With bare SV40 DNA templates, the early promoter was up to 10-fold stronger than the late promoter. The relative strengths of the early and late promoters on SV40 chromosomes were essentially independent of template concentration or length of the replicative phase of the infection. When monoclonal antibodies or antisera against T antigen (T Ag) were added to SV40 chromosomes or when T Ag, both free and chromatin bound, was removed by immunoprecipitation with anti-T, the activity of the late promoter remained essentially unchanged. Washing with 0.4 M NaCl removed T Ag from more than 90% of the mature chromosomes associated with T Ag. Transcription from the late promoter still predominated in the salt-washed T Ag-depleted chromosomes, even though there was a marked increase in early promoter activity. The depression of the early promoter could be reversed by adding the T Ag-containing extract back to the depleted chromosomes. Extraction of SV40 chromosomes with 1.5 M NaCl resulted in a decrease in the activity of the late promoter and a further increase in the activity of the early promoter so that the relative amounts of early and late RNA synthesized were similar to those for bare SV40 DNA templates. Late RNA synthesis from bare SV40 DNA templates was stimulated by high-speed supernatants prepared from nuclear extracts of SV40-infected cells but not from those of uninfected cells. Pretreatment of the supernatants with anti-T did not alter the result. Our findings indicate that the activity of the early and late SV40 promoters is regulated by at least two different mechanisms at the chromosomal level. One is mediated by a subclass of T Ag bound to SV40 chromosomes which represses early SV40 transcription but has no effect on late transcription. A second level of regulation, involving a tightly bound trans-acting chromosomal factor and a stable nucleoprotein structure, favors the late promoter over the early promoter by up to 10-fold.
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PMID:Both trans-acting factors and chromatin structure are involved in the regulation of transcription from the early and late promoters in simian virus 40 chromosomes. 298 14

Subcellular fractionation of bovine thyroid tissue by differential pelleting and isopycnic gradient centrifugation in a zonal rotor indicated that NAD(+) glycohydrolase is predominantly located and rather uniformly distributed in the plasma membrane. Comparison of NAD(+) glycohydrolase activities of intact thyroid tissue slices, functional rat thyroid cells in culture (FRT(l)) and their respective homogenates indicated that most if not all of the enzyme (catalytic site) is accessible to extracellular NAD(+). The reaction product nicotinamide was predominantly recovered from the extracellular medium. The diazonium salt of sulphanilic acid, not penetrating into intact cells, was able to decrease the activity of intact thyroid tissue slices to the same extent as in the homogenate. Under the same conditions this reagent almost completely abolished NAD(+) glycohydrolase activity associated with intact thyroid cells in culture. The triazine dye Cibacron Blue F3GA and its high-M(r) derivative Blue Dextran respectively completely eliminated or caused a severe depression in the NAD(+) glycohydrolase activity of FRT(l) cells. The enzyme could be readily solubilized from bovine thyroid membranes by detergent extraction, and was further purified by gel filtration and affinity chromatography on Blue Sepharose CL-6B. The overall procedure resulted in a 1940-fold purification (specific activity 77.6mumol of nicotinamide released/h per mg). The purified enzyme displays a K(m) of 0.40mm for beta-NAD(+), a broad pH optimum around pH7.2 (0.1 m-potassium phosphate buffer) and an apparent M(r) of 120000. Nicotinamide is an inhibitor (K(i) 1.9mm) of the non-competitive type. The second reaction product ADP-ribose acts as a competitive inhibitor (K(i) 2.7mm). The purified enzyme splits beta-NAD(+), beta-NADP(+), beta-NADH and alpha-NAD(+) at rates in the relative proportions 1:0.75:<0.02:<0.02 and exhibits transglycosidase (pyridine-base exchange) activity. Anionic phospholipids such as phosphatidylinositol and phosphatidylserine inhibit the partially purified enzyme. A stimulating effect was observed upon the addition of histones.
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PMID:Topography, purification and characterization of thyroidal NAD+ glycohydrolase. 298 95

Angiotensin converting-enzyme inhibitors cross the placenta and modify the maternal, foetal and utero-placental renin-angiotensin system. Eight cases of pregnancy in women taking captopril have been published, 7 other cases being reported in this review paper. There were one spontaneous and 2 therapeutic abortions, one of which disclosed a malformation of uncertain diagnosis and imputation. One intrauterine death at 28 weeks was probably due to the severity of the maternal disease. Two children born to mothers also treated with frusemide died of neonatal anuria. Delivery or caesarean section occurred before term in 8 cases, and there were 3 cases of neonatal respiratory distress with a favourable outcome. Finally, one mother gave birth at term to twins of normal weight. The cases with respiratory distress can be attributed to the mother's hypertension, to prematurity and/or to concomitant treatment with beta-blockers, while the cases with anuria seem to be due to inhibition of the effects of angiotensin on renal haemodynamics, with salt depression as a possible aggravating factor. Treatment with angiotensin converting enzyme inhibitors does not seem to warrant therapeutic abortion. However, these drugs are contra-indicated in pregnancy and should only be given to women wishing to become pregnant if they present with resistant and dangerous arterial hypertension. A programme of pharmacovigilance is being set up to follow up such pregnancies.
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PMID:[Inhibition of angiotensin converting enzyme in human pregnancy. 15 cases]. 300 90

Recent work with isolated blood vessels has emphasized the importance of intact endothelium when the relaxation of vascular smooth muscle is induced by acetylcholine (ACh). However, the physiologic significance of this endothelial-dependent ACh response in a complete organ circulation is unclear. We questioned whether diminished ACh vasodilation would result from damage of lung vascular endothelium and whether this response could be used as an indication of endothelial injury. We therefore induced pulmonary endothelial cell injury in one rat model by repeated injections of alpha-naphthyl thiourea (ANTU) and in a second rat model by exposing rats for 52 h to 100% oxygen at a barometric pressure of 760 torr (hyperoxia). Rats injected with Tween 80, the solvent for ANTU, or exposed to ambient Denver air served as the respective control animals. The isolated lungs of these rats were perfused with a recirculating cell- and plasma-free, physiological salt solution to study the effect of ACh or NaCl infusion on pulmonary perfusion pressure and vascular responsiveness. ANTU-treated rats demonstrated an intact vasodilatory response after ACh infusion when compared with the solvent control animals. The immediate pulmonary vasodilation after ACh infusion was slightly enhanced in the hyperoxic rat lung when compared with the rats exposed to ambient air, but there was no difference between these groups in the prolonged depression of vascular responsiveness to hypoxia or angiotensin II. Thus, in both models of lung endothelial cell injury, the pulmonary vascular responses to ACh were intact.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acetylcholine-induced pulmonary vasodilation in lung vascular injury. 300 69

The effects of methylprednisolone sodium succinate (20 mg/kg, intravenously administered) on the time course of functional recovery of myocardium following a 15-minute coronary artery occlusion period and subsequent 5 hour reperfusion period were studied in chronically instrumented, conscious dogs. In comparison to a control group, animals receiving methylprednisolone 90 minutes prior to coronary occlusion demonstrated less depression of regional segment shortening following 15 minutes of reperfusion (52 +/- 13% vs control levels of 23 +/- 7% of preocclusion values) and improved recovery at 5 hours postreperfusion (106 +/- 6% vs control levels of 54 +/- 4% of preocclusion values). In animals receiving methylprednisolone immediately prior to reperfusion, there was also similar recovery of segment shortening at 5 hours (97 +/- 3%). In contrast, dogs receiving methylprednisolone 15 minutes after the onset of reperfusion or sodium succinate (5.5 mg/kg, intravenously administered) 90 minutes prior to occlusion demonstrated no improvement in recovery of function. Experiments in dogs not subjected to coronary occlusion documented that methylprednisolone sodium succinate lacked inotropic and vasodilator properties. The results suggest that methylprednisolone administered prior to or during coronary artery occlusion but not after reperfusion enhances the functional recovery of hypokinetic, postischemic, reperfused myocardium. These effects are unrelated to any direct hemodynamic action of steroids or to the sodium succinate salt.
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PMID:Steroid-induced enhancement of functional recovery of postischemic, reperfused myocardium in conscious dogs. 305 86

Acetylcholine causes pulmonary vasodilation, but its mechanism of action is unclear. We hypothesized that acetylcholine-induced pulmonary vasodilation might be associated with prostacyclin formation. Therefore, we used isolated rat lungs perfused with a recirculating cell- and plasma-free physiological salt solution to study the effect of acetylcholine infusion on pulmonary perfusion pressure, vascular responsiveness and lung prostacyclin production. Acetylcholine (20 micrograms infused over 1 minute) caused immediate vasodilation during ongoing hypoxic vasoconstriction and prolonged depression of subsequent hypoxic and angiotensin II-induced vasoconstrictions. Both effects of acetylcholine were abolished by atropine pretreatment. The prolonged acetylcholine effect, but not the immediate response, was blocked by meclofenamate, an inhibitor of cyclooxygenase. The prolonged effect, but not the immediate response, of acetylcholine was associated with an increase in perfusate 6-keto-PGF1 alpha concentration. The acetylcholine stimulated increase in 6-keto-PGF1 alpha production was inhibited by meclofenamate and by atropine. Thus, blockade of prostacyclin production corresponded with blockade of the prolonged acetylcholine effect. In conclusion, acetylcholine caused in isolated rat lungs an immediate vasodilation and a prolonged, time-dependent depression of vascular responsiveness. Whereas both acetylcholine effects were under muscarinic receptor control, only the prolonged effect depended on the cyclooxygenase pathway and, presumably, prostacyclin synthesis.
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PMID:Acetylcholine induces vasodilation and prostacyclin synthesis in rat lungs. 308 79

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