Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Electron paramagnetic resonance spectra at 8-60 K of NADH-reduced membrane particles prepared from Paracoccus denitrificans grown anaerobically with nitrate as terminal electron acceptor show the presence of iron-sulfur centers 1-4 in the NADH-ubiquinone segment of the respiratory chain. In addition resonance lines at g = 2.058, g = 1.953 and g = 1.88 are detectable in the spectra of succinate-reduced membranes at 15 K, which are attributed to the iron-sulfur-containing nitrate reductase. 2. Sulphate-limited growth under anaerobic conditions does not affect the iron-sulfur pattern of NADH dehydrogenase or nitrate reductase. Furthermore respiratory chain-linked electron transport and its inhibition by rotenone are not influenced. These results contrast those observed for sulphate-limited growth of P. denitrificans under aerobic conditions [Eur. J. Biochem. (1977) 81, 267-275]. 3. Proton translocation studies of whole cells indicate that nitrite increases the proton conductance of the cytoplasmic membrane, resulting in a collapse of the proton gradient across the membrane. Nitrite accumulates under anaerobic growth conditions with nitrate as terminal electron acceptor; the extent of accumulation depends on the specific growth conditions. Thus the low efficiencies of respiratory chain-linked energy conservation observed during nitrate respiration [Arch. Microbiol. (1977) 112, 17-23] can be explained by the uncoupling action of nitrite.
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PMID:Anaerobic respiration and energy conservation in Paracoccus denitrificans. Functioning of iron-sulfur centers and the uncoupling effect of nitrite. 3 82

The presence of chloride conductance in basolateral membranes of proximal tubule is controversial. We measured 36Cl uptake in basolateral membranes loaded with KCl and suspended in a K(+)-free solution to create a positive intravesicular potential difference. Under these conditions, 36Cl uptake was maximal at 1 min, remained stable for at least 10 min and decreased to equilibrium levels by 60-120 min. Collapse of the voltage by valinomycin decreased 36Cl uptake by 46%, indicating the presence of K(+)-gradient-dependent chloride uptake. The chloride channel inhibitor diphenylamine-2-carboxylic acid inhibited 36Cl uptake in a dose-dependent fashion. 36Cl uptake was inhibited equally by unlabeled chloride, iodide and nitrate but not by sulfate or gluconate, indicating that the basolateral anion conductance is relatively selective. 36Cl uptake was pH independent but was calcium dependent. Phosphorylation of basolateral membranes with ATP significantly decreased 36Cl uptake, but the inhibitory effect of ATP was not further altered by exogenous cyclic AMP or the active phorbol ester PMA. These data demonstrate the presence of a relatively selective basolateral anion conductance which is regulated by pH, calcium and ATP.
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PMID:Anion channel in basolateral cortical membranes of the rabbit kidney. 133 46

The uptake of Cu+ by rat liver mitochondria is rapid and extensive. Respiration is stimulated by 10 microM Cu+ then inhibited and the inhibition could not be relieved with uncoupling agents. Collapse of the membrane potential is induced by 5-10 microM Cu+. These effects are partially inhibited by radical scavengers indicating the involvement of radical production in these events. Reduction of the GSH content and production of peroxidation products by higher amounts of Cu+ was also demonstrated. Swelling of non-respiring rat liver and heart mitochondria in sodium or lithium acetate was used to study effects of Cu+ on the Na+/H+ exchanger. Swelling is stimulated by 5-100 microM Cu+. In the presence of a radical scavenger the swelling is reduced. In sodium nitrate media diltiazem-sensitive stimulated swelling is observed. Amiloride was found to inhibit Cu(+)-induced efflux of Ca2+. At high concentrations of Cu+, a general increase in permeability was the dominant feature.
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PMID:Interaction of Cu+ with mitochondria. 166 75

Structural changes in the lens and vitreous body exposed to short-pulse Nd:YAG Q-switching laser were under study. The laser was focussed in the lens nucleus or vitreous center plane. A pulse energy was 7.1-9.3 mJ, with a total of 75-100 pulses. Cataract development was induced via the formation of cavities with the guidance spot focal plane localized in the lens nucleus plane. When the focus was in the vitreous body and the laser operated in a similar energy mode, great numbers of small cavities rapidly formed, this evidencing a shock wave propagation. Specific and structural conformational changes in the lens and vitreous protein molecules were detected by nitrate quenching of the triptophane amino acid residue fluorescence. Laser exposure was found to reduce triptophanile availability for nitrates, this evidencing protein complexes aggregation (collapse); besides, laser exposure essentially increased the amino acid residue quenching constants, which fact pointed to a decreased density of the vitreous collagen and lens crystalline negative charges (increased hydratation). These findings permit a conclusion that the shifts connected with injury to the vitreous body, with macular edema, or with detachment of the retina after exposure to Nd:YAG laser may be due to collapse of the vitreous gel liquified components.
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PMID:[Photo damage to the eye in exposure to the radiation from a Nd:YAG Q-switching laser: the physicochemical structural changes to the crystalline lens and the vitreous body]. 237 33

Lethality of anguidine (diacetoxyscirpenol) in rats and mice appears to be the result of primary or secondary cardiovascular collapse and to be related to severe tissue destruction in the gut and elsewhere. Experiments were performed in rats to examine the effect on anguidine lethality of treatment with several agents that alter gut function or toxic effects of other chemicals in the gut. Administration of atropine sulfate or methylatropine nitrate by sc injection to rats immediately following administration of an LD50 of anguidine and again 4 hr later gave modest but significant protection against anguidine lethality. The drugs were effective over a range of doses between 2.5 and 20 mg/kg, without a clear dose response, and probably were effective at doses lower than 2.5 mg/kg. S-Adenosylmethionine, 25 mg/kg, given to rats at the time of administration of an LD50 of anguidine and again 4 hr later gave some evidence of protection also. Semiquantitative evaluation of pathologic changes in the small intestine, a target of anguidine, indicated partial protection by atropine sulfate against anguidine toxicity at that site. Atropine-treated rats showed less severe damage, earlier resolution of damage, or both.
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PMID:Reduction of anguidine toxicity in rats by atropine and methylatropine. 260 47

Using quantitative biplane coronary arteriography, coronary vasomotion of normal and stenotic coronary artery segments was studied at rest and during supine bicycle exercise in 37 patients with coronary artery disease. Normal coronary arteries showed vasodilation during exercise, whereas stenotic arteries exhibited vasoconstriction. The occurrence of coronary stenosis narrowing during exercise can be explained either by a collapse of the free vessel wall due to an increase in coronary blood flow velocity (Venturi mechanism) or by insufficient production of the endothelium-derived vasorelaxing factor (endogenous nitrate). To explore further the nature of exercise-induced vasoconstriction of stenotic coronary arteries, intracoronary nitroglycerin, diltiazem or propranolol was given to a subgroup of patients prior to the exercise test. Administration of intracoronary nitroglycerin or diltiazem prevented exercise-induced vasoconstriction, probably due to the direct vasorelaxing effect of the drug on the smooth vasculature. Intracoronary administration of propranolol also prevented exercise-induced vasoconstriction, either due to a reduction in trans-stenotic pressure gradient (local beta blockade with a decrease in local coronary blood flow or an increase in distal arteriolar tone due to unopposed alpha-constrictor tone) or because of a local anesthetic effect of propranolol with a decrease in calcium influx into the smooth vasculature.
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PMID:[Coronary vasomotor activity; its significance for the therapy of angina pectoris]. 313 74

Adult female Wistar rats were injected with 1 mg/kg body weight of uranyl nitrate (UN). Evaluation of renal function, histopathology studies, and determination of plasma erythropoietin (Ep) titers after exposure to 456 mb for 16 h were performed at 1, 2, 7, 10, 15, and 21 days after drug injection. Plasma urea and creatinine concentrations markedly increased during the first seven days after injection, reaching maximal values on day 7 and decreasing thereafter. Significant increases in urine volume and significant depressions in urine osmolality also were observed; both alterations were most marked on day 7 after injection. A coagulative necrosis of the epithelium of proximal convoluted tubules, desquamation of the necrotic cells, and dilation or collapse of the tubular lumen were observed; the lesions were more marked on day 7. Plasma Ep levels in UN-treated rats exposed to hypobaria were markedly lower than in noninjected controls similarly exposed. Measurements were performed one, two, and seven days after UN injection, with maximal depression observed on day 7. These observations indicate that there is a correlation between the extent of both tubule damage and degree of renal dysfunction and plasma Ep production during exposure to hypoxia in UN-treated rats. This suggests that the renal Ep component is derived primarily from tubular cells.
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PMID:Relationship between severity of renal damage and erythropoietin production in uranyl nitrate-induced acute renal failure. 369 9

The morphological changes of the inner ear were observed after intravenous administration of 2 g/kg of urea to the guinea pigs with endolymphatic hydrops which had previously been produced by injecting 10% silver nitrate solution into the endolymphatic sac. They showed membranous collapse extensively in the saccule, moderately in the lower turns of the cochlea and less in the upper turns and the utricle. Because of these changes, it is reasonable to assume that urea is causing the endolymph to be reabsorbed in the endolymphatic duct. Furthermore, the effect of urea seemed to depend on the pathological condition of the duct which sometimes showed a varying degree of atrophied change after silver nitrate injection.
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PMID:Effect of urea on endolymphatic hydrops in guinea pigs. 408 Mar 35

The ATP-stimulated uptake of 45Ca2+ [and [3H](-)-noradrenaline ([3H]NA)] into chromaffin granules and that into mitochondria are driven by a protonic gradient delta mu H+, composed of the components delta pH (concentration gradient of protons) and delta psi (electrical potential difference). The granular ATPase pumps protons into the matrix (delta pH inside acid, delta psi positive), but the mitochondrial ATPase ejects protons from the matrix (delta pH alkaline, delta psi negative inside). To show different driving forces of uptake, the rate of the ATP-stimulated uptake of 45Ca2+ (and [3H]NA) into chromaffin granules was compared with the rate of the ATP-stimulated uptake of 45Ca2+ into mitochondria (adrenomedullary or rat liver). In the presence of nitrate, the rate of the ATP-stimulated uptake of 45Ca2+ into chromaffin granules is higher than in the presence of acetate, because the lyotropic anion nitrate stimulates the granular ATPase and increases delta pH (acid inside). Compared with nitrate, the rate of the ATP-stimulated uptake of 45Ca2+ into mitochondria is higher in the presence of the proton-carrying anion acetate, which, after permeation, provides protons for ejection by the ATPase. In the absence of ATP, a valinomycin-mediated potassium influx (delta psi inside positive) stimulates the granular uptake of [3H]NA, which has an electrogenic component, but not the granular uptake of 45Ca2+, which is electroneutral. The electrogenic uptake of 45Ca2+ into mitochondria is stimulated by a valinomycin-mediated potassium efflux (delta psi negative inside). The ATP-stimulated uptake of 45Ca2+ into chromaffin granules is sensitive to ruthenium red, suggesting a carrier-mediated mechanism of uptake, and it is sensitive to atractyloside, indicating the simultaneous uptake of ATP. After collapse of delta pH by ammonia, the ATP-stimulated uptake of 45Ca2+ into chromaffin granules is abolished, but not that into mitochondria. In the presence of ammonia, the rate of the ATP-stimulated uptake of [3H]NA is very low, and an ATP-independent uptake of 45Ca2+ into chromaffin granules is observed which is similar to the ATP-independent Ca2+/Na+ exchange at the granular membrane.
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PMID:Further characteristics of the ATP-stimulated uptake of calcium into chromaffin granules. 623 24

Acute and initial treatment with ISDN provokes arterial hypotension and orthostatic dysregulation which may persist over a period of 10 h. Collapse as a potential risk has to be taken into account in the initial phase of nitrate therapy. During chronic medication, nitrate-induced drop in arterial blood pressure and orthostatic hypotension cannot longer be seen even after high-dose application of ISDN. From a therapeutic point of view these results indicate adaptation of blood pressure regulation to chronic nitrate therapy which is unrelated to potential tolerance in the venous system.
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PMID:Nitrate-induced orthostatic hypotension and long-term circulatory adaptation. 666 30


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