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)

Norepinephrine content (microgram/g) was depressed in hearts and spleens of fasted male Holtzman rats treated intravenously with Salmonella enteritidis lipopolysaccharide (14-17 mg/kg). To investigate the mechanism of norepinephrine depletion during endotoxicosis, in vivo norepinephrine reuptake was evaluated in control and severely shocked rats using the incorporation of 3H-norepinephrine into hearts and spleens. Incorporation of 3H-norepinephrine into spleens of endotoxic rats was reduced 88%, i.e., from a control of 2309 +/- 224 dpm/gm to 270 +/- 69 dpm/gm after endotoxin. In contrast, cardiac tissue incorporation of 3H-norepinephrine was not significantly impaired, i.e., control of 11838 +/- 845 dpm/gm versus severe shock of 17783 +/- 2904 dpm/gm. In vitro analysis of total norepinephrine retained in cardiac and splenic tissue slices incubated with 3H-norepinephrine yielded results consistent with in vivo experiments: Splenic norepinephrine reuptake was significantly decreased on the order of 50% in preparations from endotoxic rats, while myocardial norepinephrine reuptake was the same in both groups. The results indicate that depression of norepinephrine reuptake is a mechanism of norepinephrine depletion in spleens but not hearts of endotoxic rats.
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PMID:Contribution of depressed reuptake to the depletion of norepinephrine from rat heart and spleen during endotoxin shock. 708 78

137 patients on maintenance dialysis were studied. All but 2 patients were ambulatory, and all patients demonstrated good to normal strength on manual motor tests. With the exception of systemic lupus erythematosus, no correlation was found between primary diagnosis and patients' fatigue ratings. Laboratory studies of hematocrit, BUN, creatinine, calcium, and phosphorus did not correlate with fatigue ratings for the majority of patients. Fatigue appeared more problematic for patients who had been dialyzing for less than 4 years. Depression was pronounced among patients who reported feeling fatigued upon arising.
Nephron 1982
PMID:The problem of fatigue in dialysis patients. 711 Apr 64

Currently accepted concepts of renal and vascular physiology are inadequate to explain the reversible increases in vascular permeability which occur during episodes of increased blood viscosity. On the basis that all basement membranes exhibit biological thixotropy, it has been suggested that basement membranes are pressure dependent. The physiological significance of increased blood viscosity lies in the associated increase in peripheral vascular resistance which develops because of altered blood rheology. In order to overcome the peripheral resistance, intravascular pressure rises, and if adequate pressures develop, plasma proteins may deform and pass through the vascular basement membrane. This is considered to be the mechanism of proteinuria. In the treatment of high blood viscosity disorders it is suggested that the immunosuppressant drug, Thiamphenicol, may be useful because of its ability to induce a reversible dose-related depression of erythropoiesis, and thereby reduce blood viscosity.
Nephron 1982
PMID:A hypothesis proposing increased blood viscosity as a cause of proteinuria and increased vascular permeability. 711 Apr 79

Norepinephrine (NE) turnover in myocardial tissue was measured in male golden hamsters (Mesocricetus auratus) during 1) continuous hypothermia, 2) rewarming from hypothermia initiated by exposure to 22 degrees C ambient, and 3) normothermic control state. Hypothermia was induced by exposure to 80% He-20% O2 atmosphere at 0 to -10 degrees C. At sequential periods after tritiated norepinephrine ([3H]NE) infusion, hamsters were killed by cervical transection and hearts were removed and analyzed for NE and [3H]NE content. Rate constants, turnover times, and turnover rates were determined from regression analysis of [3H]NE/micrograms NE tissue decay. Myocardial concentrations of NE were constant during NE-turnover measurements in each group. However, myocardial NE levels were reduced by 37% in both continuous hypothermia and rewarming from hypothermia compared with normothermic controls. NE turnover was highest during rewarming from hypothermia (0.34 micrograms.g-1.h-1), but no decay in myocardial [3H]NE was detectable during continuous hypothermia. Control animals had turnover values of 0.15 micrograms.g-1.h-1. Turnover data indicate severe depression in myocardial sympathetic nerve activity during hypothermia but a significant increase above normothermic control levels during rewarming from hypothermia.
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PMID:Myocardial norepinephrine turnover during induced hypothermia and rewarming. 722 69

Adenine dinucleotides such as beta-NAD, alpha-NAD, NADP, 3-aminopyridine adenine dinucleotide, flavin adenine dinucleotide, 3',5'-and 2',5'-adenylyladenosine mimicked the inhibitory effects of adenosine and adenine nucleotides on electrically evoked contractions of the rat and mouse isolated superfused vas deferens. The inhibitory effects were blocked by theophylline or adenosine deaminase, unaffected by the nucleotidase inhibitor alpha, beta-methylene ADP and enhanced by inhibition of adenosine deaminase. The inhibitory effects were associated with a release of purines from the vasa after preloading with [3H]adenosine. It is suggested that these compounds activate a receptor, causing the release of adenosine which is largely responsible for the inhibitions. Diadenosine pyrophosphate and triphosphate caused only depression of the vas twitch, whereas the pentaphosphate and hexaphosphate derivatives caused contraction, followed by inhibition at higher concentrations. These inhibitions were only partly reduced by theophylline or deaminase, but both contractile and inhibitory effects were enhanced by alpha, beta-methylene ADP. Noradrenaline contractions were also reduced by the higher polyphosphates. It is suggested that there may be a receptor for these dinucleotides, located at least in part postjunctionally. The pentaphosphate and hexaphosphate compounds mimicked the effects of nerve stimulation on the guinea-pig bladder, being substantially more potent than beta, gamma-methylene-ATP, and on the taenia caeci, where contraction or relaxation could be produced depending on resting tone.
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PMID:Actions of adenine dinucleotides on the vas deferens, guinea-pig taenia caeci and bladder. 731 4

The literature concerning appetite and weight changes in depressive illness is reviewed. Diminished appetite and weight loss have for about 100 years been regarded as prominent symptoms of depressive illness. A tendency for some depressives to gain weight has also been recognized. About 85% of depressives lose weight and 15% gain weight. There appears to be a tendency for weight gain to be commoner in milder depressions. Carbohydrate craving is also described in association with some depressed states. The neurochemical control of appetite in health is surveyed. Norepinephrine appears to be necessary for the intake of food, and drugs which raise intrasynaptic levels of norepinephrine stimulate feeding. Serotonin seems to be associated with satiety and in experimental animals decreased intrasynaptic levels of serotonin produce carbohydrate hunger. The neurochemical control of appetite is discussed in relation to the amine theories of depression. A number of hypotheses are drawn from this discussion.
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PMID:A neurochemical theory of appetite and weight changes in depressive states. 732 91

The role of renal hemodynamic alterations in the curtailment of renal functions was studied in uranyl acetate-induced oliguric (ORF) and nonoliguric (NORF) renal failures of rabbits. 5 days after drug injection, renal functional and morphological changes were most remarkable. A depression of Cin and elevation of serum creatinine concentration were more marked in ORF than in NORF. Renal blood flow was high as compared to controls. Cortical blood flow redistributed to the inner cortex. There was no significant difference in renal blood flow or cortical flow distribution between renal failure models. The findings suggest the minor roles of renal blood flow and cortical flow distribution in maintaining renal failure in these nephrotoxic models. Prominent tubular necrosis was found in ORF but not in NORF. Arterial inulin concentration during retrograde ureteral infusion of 14C-inulin solution was significantly high in ORF as compared to controls and NORF. However, this inulin leakage was too small to explain severely curtailed inulin clearance.
Nephron 1980
PMID:Renal hemodynamics in oliguric and nonoliguric acute renal failure of rabbits. 736 Mar

This experiment examined how inescapable tail shock alters the level of dopamine and norepinephrine within various brain regions of the rat and the relationship of these changes to the depression of motor activity produced by the shock. Following exposure to tail shock that is known to interfere with acquisition of active behavioral tasks, animals were briefly tested for spontaneous motor activity and then sacrificed for neurochemical measures. Norepinephrine and dopamine levels in the frontal cortex, brain stem, striatum, olfactory tubercle, hypothalamus, hippocampus, septum, and amygdala were measured by a sensitive radioenzymatic technique. Exposure to 45 min of tail shock did not alter motor activity significantly, but shock sessions of 60 and 75 min duration produced a marked decrease in motor activity. Levels of dopamine were found to be very little changed in all brain regions studied except for the hypothalamus, in which a substantial rise in dopamine level was observed. Norepinephrine levels, in contrast, fell in many brain regions in response to shock. The fall in norepinephrine levels observed in two brain regions was significantly correlated with the decline in motor activity (brain stem r = +0.70, hypothalamus r = +0.60). These data suggest that deficits in active motor behavior produced by shock parameters similar to those used in this study may reflect concomitant disturbances of noradrenergic function in specific brain regions.
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PMID:Stress-induced depression of motor activity correlates with regional changes in brain norepinephrine but not in dopamine. 736 96

1 The following experiments were undertaken to confirm that prostaglandin is necessary for noradrenaline to exert its full vasoconstrictor effect in rat mesenteric blood vessels. Prostaglandin release and inactivation were also studied. 2 The cyclo-oxygenase inhibitor, 5, 8, 11, 14-eicosatetraynoic acid caused a significant depression of the concentration-effect curve to noradrenaline. As with indomethacin, responses were restored to control levels by prostaglandin E2 (PGE2) but PGE2 did not restore responses to noradrenaline depressed by papaverine. 3 PGE2-like activity was released from tissues at rest, equivalent to 50 +/- 20 pg PGE2/min. The substance was probably a stable prostaglandin since activity remained on acidifying and extracting into chloroform. The increase in release stimulated by noradrenaline was reduced below resting values by indomethacin. 4 There was a net loss of 7 +/- 1 and 1 +/- 0.2 ng PGE2/min from tissues perfused with 40 and 4 ng/min PGE2 respectively. No uptake occurred at lower PGE2 perfusion rates. 5 When indomethacin was used to depress responses to noradrenaline 15(S)-15-methyl PGE2 methyl ester was 12 times more potent than PGE2 in restoring responses to control values. The cyclic endoperoxide analogue U-46619 caused only partial restoration of indomethacin-depressed responses to noradrenaline but increased perfusion pressure at 2 ng/ml and above. 6 The results confirm that endogenous prostaglandin release, possible of PGE2, is obligatory to the full vasoconstrictor effect of noradrenaline. Noradrenaline increases the amount of prostaglandin released which may be taken up and inactivated by 15-hydroxy prostaglandin dehydrogenase or beta-oxidase. U-46619 may mimic both PGE2 and thromboxane A2.
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PMID:Prostaglandin action, release and inactivation by rat isolated perfused mesenteric blood vessels. 737 46

Micropuncture and clearance studies were performed on normal untreated and polyuric lithium chloride treated rats (10-12 days). A persistent hypernatremic state quickly developed in the polyuric lithium treated rats during hydropenia resulting from an increased urinary loss of water over sodium chloride, as the fractional excretion of sodium remained at control levels. Superficial proximal tubule and loop of Henle fluid reabsorption was depressed by 8 and 17%, respectively, in lithium-treated rats during this period. By contrast, water reabsorption in the distal tubule and collecting system was significantly increased in the lithium animals, being 27% of the filtered load compared with 20% in normal rats. These results suggest that the urinary-concentrating defect induced by lithium treatment is due primarily to a depression of proximal tubule and possibly loop of Henle function, and that water reabsorption within the distal nephron may in fact be augmented: thus it is unlikely that the action of antidiuretic hormone is significantly impaired. Marked phosphaturia and hypocalciuria were also noted in the lithium-treated rats.
Nephron 1980
PMID:Effect of lithium treatment on rat renal tubule function. Evidence against impaired antidiuretic hormone action. 739 71


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