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)

Duodenal calcium absorption is depressed in alloxan and streptozotocin diabetic rats taking normal amounts to dietary vitamin D. Depression of absorption appears to be at least in part the result of altered metabolism of vitamin D with failure to form 1,25-dihydroxycholecalciferol (1,25-(OH)2D3), the vitamin D metabolite that acts directly on duodenum to stimulate calcium absorption. The South American plant Solanum malacoxylon causes extensive soft tissue calcification when ingested by cattle. An extract of this plant restores calcium absorption depressed by dietary strontium blockage of 1,25-(OH)2D3 formation in chicks. We gave an aqueous extract of S. malacoxylon to diabetic rats and restored duodenal calcium absorption to normal. These findings provide further evidence of the ability of a factor in the S. malacoxylon extract to mimic the actions of 1,25-(OH)2D3 on duodenal calcium transport and reinforce the hypothesis that abnormal vitamin D metabolism is an important determinant of depressed duodenal calcium absorption in diabetes.
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PMID:Depressed duodenal calcium absorption in the diabetic rat: restoration by Solanum malacoxylon. 12 46

Like all inhalation anesthetics, halothane (CF3CHBrCl) has a dose-dependent negative inotropic effect on cardiac muscle. The mechanism of the action has not been determined, although effects on glycolysis, mitochondrial respiration and calcium kinetics, and sarcoplasmic reticulum ATPase activity have been suggested. Previous studies of the effect of halothane on the ATPase of contractile protein suffered from design and dosing defects. We have measured ATP splitting by canine cardiac natural actomyosin using extraction and equilibration procedures described previously (Honig, C. R. and Reddy, Y. C. 1973, J. Pharmacol. 184: 330-338). Drug dosing calculations were facilitated by measurement of the partition coefficient of halothane in protein. Halothane shifted the Ca++ concentration effect curve for actomyosin ATPase activity to the right. The maximum depression occurred at pCa 7.0 or 6.5. The effect was dose dependent with less than 10 percent depression at threshold and 50-60 percent depression at peak. Enzyme inhibition was antagonized by high Ca++ concentration, and was reversed by removing halothane from the reaction mixture. We suggest that inhibition of ATP utilization by the contractile system may be a mechanism of the in vivo myocardial depression produced by halothane.
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PMID:Halothane decreases actomyosin ATPase activity: a possible mechanism of the negative inotropic effect. 12 60

Dialysis rates of cholesterol, calcium chloride dihydrate and of their mixture in 90% aqueous dioxane through Visking cellulose membrane were characterized by half-escape times (t1/2) of 2.2, 1.0 and 10.5 hours, respectively. Slow dialysis rate observed with the mixture was due to complex formation between four molecules of cholesterol and two molecules of calcium chloride dihydrate, molecular weight 1800 to 2000. The association constant for this complex in 90% aqueous dioxane was estimated to be 3.9 X 10(14). Rates of dialysis obtained with a natural protein membrane were in the reverse order to those obtained with cellulose membrane. Half-escape times for cholesterol, calcium chloride dihydrate and for their mixture were 0.6, 6.7 and 1.4 hours, respectively. Determinations of milliosmolality of the three solutions by freezing point depression indicated that in the mixture there were fewer osmotically active particles than in their separate solutions of the same molarity, also suggesting formation of the complex which was detected by dialysis experiments.
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PMID:Interaction between cholesterol and calcium ions in solution. 13 5

The Km value for the dog heart (Na+-K+)-ATPase was 0.31 mM (MgATP), whereas the values for the concentrations of K+ and Na+ varied from 1.2 to 2.7 mM and 12 to 20 mM for half-maximal activation, respectively. The concentrations of ouabain and calcium for 50 percent inhibition of (Na+-K+)-ATPase activity varied from 2.4 to 3.2 muM and 0.5 to 1.2 mM, respectively, the inhibitory effects of these agents were pH dependent. This preparation bound about 50 nmoles of 1-anilino-8-napthaline sulfonate (ANS)/mg of protein and exhibited fluorescence attributable to the ANS-enzyme complex. Cations such as Na+,K+,Ca++, and Mg++ increased ANS-enzyme fluorescence intensity and the number of ANS binding sites but decreased the apparent ANS binding constant. The enzyme activity, ANS binding, and ANS-enzyme fluorescence were decreased by phospholipase A, phospholipase C, and trypsin treatments. Although ouabain inhibited enzyme activity and ANS-enzyme fluorescence markedly, it caused only a slight depression in ANS binding. These results extend support for the allosteric nature of the cardiac (Na+-K+)-ATPase and provide evidence for conformational changes during its activation by Na+ and K+.
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PMID:Characterization of partially purified heart sarcolemmal Na+-K+-stimulated ATPase. 13 Jun 58

To examine the role of changes in calcium transport by subcellular particles in the pathogenesis of contractile failure due to oxygen lack, both mitochondrial and microsomal fractions were obtained from the isolated hypoxic rat hearts and their calcium binding and uptake abilities were determined by the Millipore filtration technique. The contractile force decreased by about 40, 60 and 70% of the control within 5, 10 and 30 min respectively, of perfusing the heart with hypoxic medium containing glucose. In hearts perfused for 10 min with hypoxic medium containing glucose, calcium binding and uptake by the microsomal fraction decreased significantly. However, mitochondrial calcium binding, but not uptake, decreased significantly on perfusing the hearts with hypoxic medium containing glucose for 20 to 30 min when the microsomal calcium transport was markedly depressed. Reduction in contractile force, calcium binding and uptake by the microsomal fraction as well as calcium binding by mitochondria of hearts made hypoxic for 30 min recovered towards normal upon reperfusion with control medium for 15 min. On the other hand, omitting glucose from the hypoxic medium significantly decreased calcium binding by mitochondrial and microsomal fractions within 10 min of perfusion in comparison to the control and accelerated the effects of hypoxia upon contractile force and microsomal calcium uptake. In contrast to the hypoxic hearts, the mitochondrial calcium uptake decreased significantly and the magnitude of depression in the microsomal calcium binding was appreciably greater in hearts made to fail to a comparable degree upon perfusion with substrate-free medium. The observed defects in calcium transporting properties of microsomal and mitochondrial membranes appear secondary to the contactile failure in hypoxic hearts.
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PMID:Excitation-contraction coupling in heart. XIX. Effect of hypoxia on calcium transport by subcellular particles in the isolated perfused rat heart. 13 Sep 66

We studied hearts from sham-operated and uninfected catheterized rabbits as well as from rabbits at early and late stages of cardiomyopathy and failure after 3 and 6 days of infection with Streptococcus viridans. No ultrastructural abnormalities or biochemical changes in membrane and myofibrillar activities were seen in 3-day uninfected hearts. In 6-day uninfected hearts there were decreased sarcolemmal M2+ ATPase, Na+-K+ ATPase, adenylate cyclase and calcium binding, microsomal calcium binding and uptake, and myofibrillar Ca2+-stimulated ATPase as well as increased mitochondrial calcium uptake. Slight ultrastructural changes also were apparent in 6-day uninfected hearts. At both early and late stages of infective cardiomyopathy and failure there were varying degrees of depression in sarcolemmal Mg2+ ATPase, Na+-K+ ATPase, adenylate cyclase and calcium binding, microsomal calcium binding, calcium uptake and basal ATPase, and myofibrillar Ca2+-stimulated ATPase activities. However, sarcolemmal Ca2+ ATPase and myofibrillar Mg2+ ATPase activities were decreased only after 6 days of infection. Mitochondrial calcium binding and uptake were increased in early stages but decreased in late stages of disease. Furthermore in infected hearts there were defects in mitrochondrial respiration and phosphorylation. Generalized severe myocardial cell damage involving myofibrils, mitochondria, and the sarcotubular system was seen only in late stages of infection. The results demonstrate impairment of different membrane and contractile protein functions as well as ultrastructural abnormalities in bacterial cardiomyopathic hearts which were absent or of lesser magnitude in hearts with only hypertrophy. The findings reported here suggest to use that there is an association between heart failure and changes in function of cellular components during bacterial infective cardiomyopathy.
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PMID:Abnormalities in heart membranes and myofibrils during bacterial infective cardiomyopathy in the rabbit. 13 11

Subcellular fractions in hearts from rats with severe acute uremia (24 hours after total nephrectomy) and moderate chronic uremia (2 weeks after five sixths nephrectomy) were studied and compared with preparations from acute and chronic sham-operated rats, respectively. Calcium- and magnesium-sensitive actomyosin adenosine triphosphatase (ATPase) activities were normal in both groups. Acute uremia was associated with a significant depression of sarcolemmal Na+,K+ ATPase activity. Calcium transport by fragmented sarcoplasmic reticulum was also depressed in the presence and absence of oxalate in acute uremia. Mitochondrial calcium transport and adenosine triphosphate (ATP) and creatine phosphate (CP) concentrations were normal in these animals. Chronic uremic animals showed no abnormal subcellular mechanisms. These data suggest a direct effect of acute uremia on some membrane functions in myocardial cells. The discrepancies observed between acute and chronic uremic groups may be due to a different degree of uremic state. The observation of depressed calcium transport by fragmented sarcoplasmic reticulum (FSR) in acute uremic hearts which were previously shown to have increased contractile reserve suggests that studies of calcium transport in FSR may not always truly reflect the contractile capacity of the heart.
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PMID:Studies of subcellular control factors in hearts of uremic rats. 13 36

Control and streptozotocin diabetic rats were studied at 5 and 12 days after induction of diabetes. Strontium absorption was measured by in situ perfusion of duodenum and ileum. Duodenal absorptive capacity (absorption per unit length) and absorptive specific activity (absorption per gram of dry weight mucosa) were depressed. Depression was present both at 5 days, when mucosal growth is similar in controls and diabetics, and at 12 days, when mucosal growth is 50% greater in diabetics. Effects of diabetes on ileal absorption were minimal in comparison with effects on duodenum. This depression of duodenal strontium absorption in the diabetic rat is analogous to effects of diabetes on calcium absorption and may be mediated by abnormal vitamin D metabolism.
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PMID:Effects of experimental diabetes on intestinal strontium absorption in the rat. 13 63

The Ca2+-activated myosin ATPase and the amino acid compositions of actin and myosin were determined for preparations from chronically failing dog hearts. Hypertrophy and congestive heart failure were produced by combined tricuspid valve insufficiency and pulmonary artery stenosis. Control, shamoperated, and noncardiac circulatory failure (inferior vena cava constriction) dogs also were studied. All hearts were divided into right ventricle, septum and left ventricle and each sample was individually analyzed. Calcium-activated ATPase decreased in the failing hearts and showed a distinct gradient of depression from right to left ventricles. There were no changes in ATPase activity among the other groups. The amino acid composition of actin was the same regardless of origin. The amino acid composition of myosin was unaltered except that cystine/2 residues were markedly decreased in failing heart myosin. The same gradient of depression was present as was found for Ca2+-activated myosin ATPase. This study suggests that protein metabolism is abnormal and that altered proteins are produced in hypertrophy and congestive heart failure. It appears that these changes do not affect all proteins, since actin was normal by the parameters studied. It is clear that the stressed ventricle is the most severely involved, but the entire heart is altered to some degree. Thus, we conclude that altered protein metabolism may be an important primary factor in the genesis of heart failure.
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PMID:The amino acid composition of actin and myosin and Ca2+-activated myosin adenosine triphosphatase in chronic canine congestive heart failure. 13 12

The effects of iontophoretically applied Na+-, K+-dependent adenosinetriphosphatase (Na+,K+-ATPase) (EC 3.6.1.3) inhibitors (ouabain, digitoxin, digitoxigenin, strophanthin K, strophanthidin, thevetin A and B, ethacrynate, and harmaline) on the depression of rat cerebral cortical neurones by noradrenaline, 5-hydroxytryptamine, and histamine have been studied. The inhibitors antagonized depressions of spontaneously active neurones evoked by these amines, but not those evoked by gamma-aminobutyric acid, adenosine, adenosine 5'-monophosphate, or calcium. The antagonistic potencies of the various inhibitors appeared to be proportional to their known potencies as inhibitors of Na+, K+-ATPase. The data therefore support the hypothesis that amines depress central neurones by activating an electrogenic sodium pump.
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PMID:Antagonism of biogenic amine-induced depression of cerebral cortical neurones by Na+, K+-ATPase in inhibitors. 14 20


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