Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severity of renal injury and recovery of function in acute renal failure (ARF) are strongly related not only to the magnitude and nature of ARF insult but also to numerous factors in the host which govern renal susceptibility to the insult and repair of renal lesion. Prior ARF affords resistance to a rechallenge with the same or different ARF insult. The mechanisms for this acquired resistance to ARF have not been well established, but suggested mechanisms include (a) increased resistance of regenerated tubular epithelial cells to a rechallenge, (b) glomerular refractoriness to vasoactive substances, (c) failure of damaged kidney to concentrate the toxic substance, (d) enhanced antioxidant enzyme activity in glomeruli, and (e) increased Na(+)-K(+)-ATPase activity in regenerated tubular epithelial cells. Controversy still exists regarding roles of these factors in the resistance to renal failure. Functional and morphologic recovery of postischemic kidney is enhanced by antecedent unilateral nephrectomy but delayed in the presence of the contralateral kidney. The mechanisms for the effect of uninephrectomy remain unsettled. Recent studies suggest contributions of changes in preglomerular vascular resistance; alterations in the environment which follow ischemia to all functioning excretory renal tissues; and altered production and release of vasoactive substances such as angiotensin, endothelin, thromboxane, and atrial natriuretic peptide.
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PMID:Factors affecting severity of renal injury and recovery of function in acute renal failure. 132 11

Na-coupled D-glucose transport in rabbits with cis-diamminedichloride platinum (CDDP; cisplatin) induced acute renal failure (ARF) has been studied. ARF occurred at 3 days after injection of CDDP (3 mg/kg i.v.). Na-coupled D-glucose transport into brush-border membrane vesicles (BBMV) from both outer cortex (OC) and outer medulla (OM) of ARF rabbits under zero-trans condition was decreased. Increased Km (i.e., decreased affinity of transport carrier for D-glucose) in OC and decreased Vmax (i.e., decreased number of glucose carrier) in OM were observed in CDDP-induced ARF rabbits. Decrease glucose transport was also observed under equilibrium exchange condition. Intravesicular volume of BBMV from OC and OM of ARF rabbits was decreased. In homogenate and BBMV from OC and OM of ARF rabbits, activities of gamma-glutamyl transpeptidase and alkaline phosphatase (marker enzymes of brush-border membrane) were decreased. Activities of succinate dehydrogenase, glucose-6-phosphatase, and Na-K ATPase (marker enzymes of mitochondria, endoplasmic reticulum, and basal lateral membrane, respectively) were not affected by CDDP administration. These results suggested that one of the main target sites of CDDP in kidney is brush-border membrane (BBM) along the proximal tubule, that is, not only Na-coupled D-glucose transport carrier protein but also other proteins in BBM.
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PMID:Decreased sodium dependent D-glucose transport across renal brush-border membranes in cis-diamminedichloride platinum induced acute renal failure. 156 86

Dopamine receptors of DA-1 and DA-2 subtypes are localized in various regions within the kidney including the renal vasculature (DA-1) as well as sympathetic nerve terminals innervating the renal blood vessels (DA-2). More recent studies using receptor-ligand binding and receptor autoradiography have shown that DA-1 receptors are localized at both the luminal and basolateral membranes at the level of the proximal tubules. Activation of these DA-1 receptors by dopamine and by selective DA-1 receptor agonists results in natriuresis and diuresis. The cellular signaling mechanisms responsible for this response appear to be DA-1 receptor-induced activation of adenylate cyclase and phospholipase C, which via the generation of various intracellular messenger systems cause inhibition of Na(+)-H+ antiport (luminal) and Na+, K(+)-ATPase (basolateral), respectively. Both of these events consequently inhibit sodium reabsorption leading to natriuresis and diuresis. It is also known that dopamine can be synthesized within proximal tubular cells from L-dopa, which is taken up from the tubular lumen, and this locally produced dopamine plays an important role in the regulation of sodium excretion particularly during increases in sodium intake. Furthermore, a defect in the renal dopaminergic mechanism may be one of the pathogenic factors in certain forms of hypertension. Finally, whereas DA-1 receptor agonists are shown to be of therapeutic benefit in the treatment of hypertension, heart failure, and acute renal failure, some selective DA-2 receptor agonists are effective antihypertensive agents.
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PMID:Anatomical distribution and function of dopamine receptors in the kidney. 168 44

Potassium depletion can potentiate several experimental models of acute renal failure. It causes renal vasoconstriction, probably under the influence of vasoconstrictor prostaglandins and angiotensin II, and causes a reduction in vasodilatory prostaglandins. Aminoglycoside nephrotoxicity in experimental animals and in man causes a reduction in serum potassium and in animals it enhances the functional and histological damage produced by aminoglycosides. Chronic potassium loading protects against mercuric chloride, uranyl nitrate, and gentamicin models of acute renal failure. In the gentamicin model, protection is associated with a stimulation of renal cortical Na-K-ATPase activity and a reduction in the level of gentamicin accumulated in cortical tissue. In the clinical setting, potassium deficiency should be avoided in patients at risk for acute renal failure. However, potassium loading should also be avoided, since a falling glomerular filtration rate in the presence of a potassium load could result in potentially serious hyperkalemia.
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PMID:Role of potassium in the pathogenesis of acute renal failure. 175 17

Ischemic injury results in proximal tubule (PT) dysfunction and loss of surface membrane (SM) polarity. Since epithelial vectorial transport requires SM polarity, we set out to determine if correction of renal cortical PT dysfunction following ischemia was dependent on the reestablishment of SM polarity. Acute renal failure was induced using a bilateral 50-min pedicle clamp. Serum creatinine and fractional sodium excretion were maximal on day 1, remained elevated on day 3, and returned toward base line by day 8. PT cellular ultrastructure was normal by day 3. Despite rapid morphological recovery, ischemia resulted in a prolonged defect in glucose reabsorption. The delayed recovery of normal glucose handling closely paralleled the slow normalization of apical membrane lipid polarity. Na+-K+-ATPase polarity was also lost secondary to ischemia as demonstrated cytochemically and biochemically by the redistribution of Na+-K+-ATPase to the apical membrane. The time required to reestablish normal Na+-K+-ATPase polarity (8 days) paralleled the recovery of normal PT Na+ reabsorption (8 days), as assessed by fractional lithium clearances. This finding supports the hypothesis that apical Na+-K+-ATPase is in part responsible for reduced Na+ reabsorption following ischemic injury. In summary, these data suggest that functional recovery of PT glucose and Na+ reabsorption following a reversible ischemic insult requires not only morphological recovery, but also the reestablishment of surface membrane lipid and protein polarity.
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PMID:Epithelial polarity following ischemia: a requirement for normal cell function. 253 79

Gentamicin nephrotoxicity increases renal cortex calcium and sodium and decreases renal cortex Na-K-ATPase activity. Human acute renal failure is accompanied by an increase in parathyroid hormone (PTH), a hormone that stimulates calcium uptake by tissues, and by a decrease in thyroid hormone, a hormone that increases renal cortex Na-K-ATPase activity. This study evaluated the role of extracellular calcium, PTH, and thyroxine in the pathogenesis of gentamicin nephrotoxicity. Chronically parathyroidectomized hypocalcemic rats (PTXG) given gentamicin (30 mg/kg s.c. twice daily for 8 days) were not protected from renal failure when compared with intact rats given gentamicin (NG), serum creatinine being 4.4 +/- 1.0 and 3.7 +/- 0.7 mg/dl, respectively, compared with normals (N), 1.2 +/- 0.1 mg/dl. Rats given thyroxine (10 micrograms/100 g body wt for 10 days) before and during gentamicin (PTXT4G) had a serum creatinine not significantly different from normals, 2.1 +/- 0.4 mg/dl. Plasma T4 was reduced in PTXG, NG, and PTXT4G compared with N, but the value for PTXT4G was significantly higher than for either PTXG or NG. Renal cortex Na-K-ATPase activity (mumol Pi X mg prot-1 X h-1) was lower in PTXG (2.3 +/- 0.2) and NG (2.4 +/- 0.5) compared with N (3.7 +/- 0.1), but activity was not reduced in PTXT4G (3.2 +/- 0.2) Thyroxine was protective also against gentamicin nephrotoxicity in intact rats. Clearance and excretion studies indicated that this protection did not result from an increase in glomerular filtration rate, filtered load of calcium, or urinary calcium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of thyroxine but not parathyroidectomy on gentamicin nephrotoxicity. 257 82

The exact mechanism of gentamicin-induced acute renal failure is presently unknown; various mechanisms have been proposed but there is no proposed commonality between them. In animals, dietary calcium loading and L-thyroxine administration have been shown to ameliorate toxicity, with again no common process. A mechanism of competitive displacement of calcium and other cations from anionic phospholipids at the plasma and organelle membrane level, resulting in a decrease in Na+ -K+ ATPase, adenylate cyclase, mitochondrial function and ATP production, protein synthesis, solute reabsorption and overall cellular function is proposed. A further proposal is dietary calcium loading and thyroxine (which increases intracellular calcium) reverse gentamicin-induced acute renal failure by increasing the calcium and solute flux, thereby competitively inhibiting the primary lesion: anionic phospholipid binding.
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PMID:Model of gentamicin-induced nephrotoxicity and its amelioration by calcium and thyroxine. 268 48

Transport of D-glucose, p-aminohippurate and tetraethylammonium has been studied using renal brush border membrane vesicles isolated from rats with uranyl nitrate-induced acute renal failure (ARF). Initial rate and overshoot magnitude of Na+ gradient-dependent D-glucose uptake were decreased in brush border membrane vesicles from ARF rats compared with normal rats, although there was no significant difference on D-glucose uptake in the presence of equilibrated Na+ between normal and ARF rats. Uptake of p-aminohippurate by membrane vesicles from ARF rats did not differ from normal membrane vesicles. Uptake of tetraethylammonium with or without an H+ gradient was decreased in membrane vesicles from ARF rats compared with normal rats. Dissipation rate of H+ gradient across brush border membranes did not differ between both groups. In vitro incubation of normal brush border membrane vesicles with uranyl nitrate caused no alteration in any substrate transport. However, enzyme activities such as (Na+ + K+)-adenosine triphosphatase in renal cortical homogenate were inhibited markedly in the presence of uranyl nitrate. These results suggest that uranyl nitrate-induced ARF caused alterations in the transport properties of renal brush border membranes and that these transport dysfunctions were not due to the direct effect of uranyl nitrate, but could be secondarily induced after the impairment of the integrity for tubular cells.
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PMID:Transport of p-aminohippurate, tetraethylammonium and D-glucose in renal brush border membranes from rats with acute renal failure. 298 96

Acute renal failure (ARF) was experimentally induced in rats and the specific activity of mucosal Na-K-ATPase activity in segments of the small intestine and colon was measured. Bilateral nephrectomy (BN) resulted in a significant evaluation of the enzyme activity in all segments examined. With an additional procedure of adrenalectomy (BN + Ax), the enzyme activity failed to show any increase in ARF rats produced by BN. However, a supplementation of a maintenance dose of dexamethasone to adrenalectomized ARF rats (BN + Ax + DM 10) resulted in a significant resumption of the activity in all intestinal segments, although its increase was insignificant in the duodenum. Addition of a high dose of DOCA (BN + Ax + DOCA 500) was effective in increasing the enzyme activity only in the colon but not in the small intestine. With a high dose of DM or a maintenance dose of DM plus a high dose of DOCA (BN + Ax + DM 30 or BN + Ax + DM 10 + DOCA 500), there was an increase in the enzyme activity of all intestinal segments. In ARF rats induced by bilateral lower ureteral ligation (BLUL), the enzyme activity did not show any increase at all. Addition of a high dose of DOCA to this animal model (BLUL + DOCA 500) brought about the increase of the enzyme activity in the intestinal segments but for the jejunum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of intestinal adaptation in rats with acute renal failure. 299 57

Digitalis-like factors were assayed by radioimmunoassay of digoxin in 6 bile samples obtained from patients at autopsy and in plasma from three patients with combined hepatic and acute renal failure. None of the patients received digoxin. Digitalis like factor values in bile samples were 23 to 85 nmol digoxin equivalents/1. Bile salt concentrations ranged from 38-104 mmol/l in the bile and 28-184 mumol/l in the plasma of these subjects. Bile, plasma digitalis like factor extracts and bile salt standards (0.1-3 mM) showed concentration dependent displacement of [125I]-digoxin from digoxin antibody, inhibition of hog brain Na,K-ATPase and displacement of [3H]-ouabain from Na,K-ATPase. The concentration-displacement curves suggest that bile salts could account for 50-79% of the total digitalis like factors in the six bile samples and 2-7% in the plasma of the three patients. High performance liquid chromatographic fractionation of a bile sample showed digitalis like factor peaks co-eluating with standards of tauro- and glycocholate, tauro- and glycochenodeoxycholate and tauro- and glycodeoxycholate. These bile salt peaks accounted for 78% of the total digitalis like factors in all high performance liquid chromatographic peaks in bile, but only 7% of the total digitalis like factor activity in all high performance liquid chromatographic peaks in an extract of plasma from one of the patients with hepatic and renal failure. The bile salts appear to be examples of endogenous digitalis like compounds which do not act by simple competitive ligand binding to antidigoxin antibody and Na,K-ATPase. They make an important contribution to digitalis like factor activity in bile, but not in plasma.
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PMID:Bile salts as endogenous digitalis like factors. 301 98


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