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1. |
Editorial |
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Current Opinion in Nephrology and Hypertension,
Volume 1,
Issue 1,
1992,
Page 1-1
Barry Brenner,
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ISSN:1062-4821
出版商:OVID
年代:1992
数据来源: OVID
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2. |
Uremic syndrome revisited: a pathogenetic role for retained endogenous inhibitors of nitric oxide synthesis |
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Current Opinion in Nephrology and Hypertension,
Volume 1,
Issue 1,
1992,
Page 3-7
Barry Brenner,
Alan Yu,
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PDF (457KB)
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ISSN:1062-4821
出版商:OVID
年代:1992
数据来源: OVID
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3. |
Molecular cell biology and physiology of solute transport |
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Current Opinion in Nephrology and Hypertension,
Volume 1,
Issue 1,
1992,
Page 9-11
Steven Hebert,
Steven Gullans,
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PDF (241KB)
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ISSN:1062-4821
出版商:OVID
年代:1992
数据来源: OVID
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4. |
The molecular biology of mammalian glucose transporters |
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Current Opinion in Nephrology and Hypertension,
Volume 1,
Issue 1,
1992,
Page 12-20
Mike Mueckler,
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PDF (902KB)
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摘要:
Recent advances concerning the function and regulation of the facilitative and sodium-dependent glucose transport proteins are discussed. Physiologic roles have been proposed for GLUT3 and CLUT5 in the brain and intestine, respectively. Cell biologists are beginning to elucidate the subcellular trafficking pathways of GLUT4 in insulin-responsive cells. New members of the SGLT family, including a sodium-nucleoside cotransporter, have been identified.
ISSN:1062-4821
出版商:OVID
年代:1992
数据来源: OVID
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5. |
ATP-sensitive potassium channels in physiology, pathophysiology, and pharmacology |
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Current Opinion in Nephrology and Hypertension,
Volume 1,
Issue 1,
1992,
Page 21-33
Stanley Misler,
Gerhard Giebisch,
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摘要:
Potassium-selective ion channels, whose activity is inhibited by micromolar to millimolar concentrations of ATP presented at the cytoplasmic ATP-sensitive K+(K+[ATP]) surface, have been found in a variety of cell types. These “K+(ATP) channels” have emerged as significant targets for physiologic as well as pharmacologic modulation of cell processes. In insulin-secreting β cells of the pancreatic islet, closure of these channels on presentation of a metabolite secretogogue, such as glucose, or an oral hypoglycemic sulfonylurea, results in cell depolarization and triggers electrical activity. Ultimately, this results in Ca2+ entry and Ca2+-dependent exocytosis of insulin granules. In myocytes, opening of K+(ATP) channels during hypoxia or metabolite deprivation or with exposure to a new class of K+ channel opener drugs results in cell hyperpolarization and myocyte relaxation. This contributes to vasodilation. In renal tubule cells, K+(ATP) channels contribute to cell potassium balance during vectorial bulk solute transfer by the proximal tubule as well as net urinary potassium secretion by the distal nephron. Agents that modulate the activity of these K+(ATP) channels in epithelial cells may prove to be useful as K+-sparing diuretics.
ISSN:1062-4821
出版商:OVID
年代:1992
数据来源: OVID
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6. |
The molecular biology of chloride channels |
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Current Opinion in Nephrology and Hypertension,
Volume 1,
Issue 1,
1992,
Page 34-42
John Riordan,
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摘要:
The molecular biology of chloride channels is a new field, having begun only 5 years ago with the cloning, on the basis of partial amino acid sequence information, of complementary DNAs for subunits of the neuronal glycine and γ-aminobutyric acid-receptor channels. The sequences of these subunits that form heterooligomeric channels revealed a general similarity with the structural motif employed by the well-studied and previously cloned nicotinic acetylcholine-receptor subunits. The principal distinguishing feature was the rings of positively charged residues within the loops separating the putative transmembrane helices of the new chloride selective channels. A great diversity of subunit types with specific functional and pharmacologic properties as well as localizations within the central nervous system have been identified and cloned. Chloride channels are known to play an important role in both secretion and reabsorption of salt and fluid across wet epithelia, and the cystic fibrosis transmembrane conductance regulator, cloned by genetic means, has been shown to be centrally involved in both of these processes. It is regulated by a complex mechanism involving both ATP binding and phosphorylation at multiple sites. Expression cloning techniques have yielded a voltage-gated family of channels with a large number of potential membrane spanning segments; one member is responsible for the resting potential of skeletal muscle. An entirely different low molecular weight-voltage-gated channel, possibly regulated by osmolarity changes, is the most recent chloride channel to be cloned. It almost certainly will not be the last.
ISSN:1062-4821
出版商:OVID
年代:1992
数据来源: OVID
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7. |
Osmolytes |
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Current Opinion in Nephrology and Hypertension,
Volume 1,
Issue 1,
1992,
Page 43-52
Franz Beck,
Michael Schmolke,
Walter Guder,
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摘要:
The cells of the renal medulla osmotically adapt to chronic alterations in extracellular tonicity by appropriate changes in the intracellular contents of organic osmoeffectors. The major organic osmolytes are glycerophosphorylcholine, betaine, myo-inositol, sorbitol, and, possibly, taurine. When the concentrations of poorly permeant external solutes are acutely reduced, cells that have been adapted to high tonicities rapidly release organic osmolytes via specific transmembrane transport pathways. In contrast, when medullary cells are depleted of organic osmolytes, osmolyte accumulation on acute elevation of external tonicity is slow and involves stimulation of uptake, intracellular de novo synthesis, or inhibition of intracellular degradation, and is preceded by increased intracellular electrolyte concentrations. The available evidence suggests that this rise in intracellular ionic strength plays an important role in the initiation of those processes responsible for full adaptation of renal medullary cells to high tonicities. Recently, complementary DNAs encoding a myoinositol and a betaine transporter have been isolated.
ISSN:1062-4821
出版商:OVID
年代:1992
数据来源: OVID
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8. |
Cellular and molecular mechanisms of renal development and tubulogenesis |
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Current Opinion in Nephrology and Hypertension,
Volume 1,
Issue 1,
1992,
Page 53-58
Qais Al-Awqati,
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摘要:
Recent advances in the basic mechanisms of developmental biology have started to shed new light on the mechanisms of nephrogenesis. The kidney is the only epithelial organ that starts as mesenchyme and converts to epithelium. It appears that the mesenchyme is composed of stem cells that are able to form glomeruli and proximal and distal tubules under the inductive influences of the ureteric bud. Epithelial cells cultured in a three-dimensional matrix could be induced to form tubules under the influence of a soluble factor from fibroblasts. This factor was identified as scatter factor or hepatocyte growth factor. Polycystic kidney disease appears to be a developmental renal disease in which a basolateral protein, the Na/K ATPase, is mistargeted to the apical and lateral membranes.
ISSN:1062-4821
出版商:OVID
年代:1992
数据来源: OVID
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9. |
Renal epithelial cell polarity |
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Current Opinion in Nephrology and Hypertension,
Volume 1,
Issue 1,
1992,
Page 59-67
W James Nelson,
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摘要:
Recent cell biologic studies of protein trafficking, sorting, and distribution in polarized renal epithelial cells have begun to provide important new insights into the mechanisms involved in generating and maintaining cell surface polarity. Advances in this field have been rapid in the last year, due in part to the development of new approaches to analyzing protein delivery and distribution in polarized renal cells grown in vitro. Sorting signals within apical and basal-lateral membrane proteins have been described that may be involved in the segregation of proteins into different populations of transport vesicles in the trans-Golgi network; the nature of these signals has provided insight into the mechanisms involved. Elements of the cytoskeleton appear to be involved in the delivery of these transport vesicles to the appropriate membrane domain (microtubules) and in the retention of specific proteins in the correct membrane domain (membrane skeleton). Finally, detailed analysis of two prominent renal diseases, ischemia and polycystic kidney disease, indicates that abnormalities in the regulation of membrane protein distribution may be a contributing factor in generating the disease state.
ISSN:1062-4821
出版商:OVID
年代:1992
数据来源: OVID
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10. |
Defects in membrane transport of ions as possible pathogenic factors in hypertension |
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Current Opinion in Nephrology and Hypertension,
Volume 1,
Issue 1,
1992,
Page 68-72
Abraham Aviv,
Norman Lasker,
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PDF (485KB)
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摘要:
Although abnormalities in cellular ion transport have been shown in a variety of cells of essential hypertensives, the mechanistic link between these abnormalities and elevated blood pressure is poorly understood. Reduced sodium-potassium ATPase activity, with and without elevated levels of a circulating inhibitor of this transport system, has been reported by a number of studies. The recent characterization of the endogenous ouabain or its isomer will facilitate the testing of the hypothesis that salt-sensitive essential hypertension relates to higher levels of this factor. The erythrocyte sodium-lithium countertransport may serve as a marker for a subpopulation of essential hypertensives. However, this transport system has no physiologic counterpart and thus does not provide insight into mechanisms associated with altered cellular ionic homeostasis in essential hypertension. Increased activity of the sodium-hydrogen antiport in essential hypertension relates to an alkaline shift in the cytosolic pH set-point for activation of this transport system. This process may reflect increased cytosolic free calcium concentration with or without augmented protein kinase C activity.
ISSN:1062-4821
出版商:OVID
年代:1992
数据来源: OVID
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