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  • 1
    Electronic Resource
    Electronic Resource
    Angiotensinase A gene expression and enzyme activity in isolated glomeruli of diabetic rats (1996)
    Springer
    Diabetologia 39 (1996), S. 275-280 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic nephropathy ; renin angiotensin system ; angiotensinase A
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary One of the characteristics of early diabetic nephropathy is glomerular hyperfiltration and hyperperfusion. Many factors have been suggested to induce glomerular hyperperfusion among which are an increased production of vasodilatory prostanoids, an increased synthesis of nitric oxide, a reduced responsiveness of afferent glomerular arterioles to vasoconstrictor stimuli due to diabetic metabolic disturbances and a decreased receptor density for angiotensin II. It has been known for years that angiotensin II is formed locally due to the local activation of the renin angiotensin system. The local angiotensin II concentration, however, is not only regulated by the synthesis rate but also by the local degradation through activation of an aminopeptidase. The main finding of the present study was that the mRNA expression and activity of the angiotensin II degrading enzyme, angiotensinase A, was increased twofold in diabetic rats at 5 weeks and that the increase in mRNA expression was suppressed by insulin therapy and short-term treatment with the angiotensin II antagonist saralasin, whereas angiotensinase A enzyme activity was only reduced by saralasin and not by insulin. These results demonstrate that the angiotensin II degrading exopeptidase angiotensinase A is activated in diabetic glomeruli. This increased activity may be an additional mechanism to explain glomerular hyperfiltration and hyperperfusion in early diabetic nephropathy. [Diabetologia (1996) 39: 275–280]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418342
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Angiotensinase A gene expression and enzyme activity in isolated glomeruli of diabetic rats (1996)
    Springer
    Diabetologia 39 (1996), S. 275-280 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic nephropathy ; renin angiotensin system ; angiotensinase A
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary One of the characteristics of early diabetic nephropathy is glomerular hyperfiltration and hyperperfusion. Many factors have been suggested to induce glomerular hyperperfusion among which are an increased production of vasodilatory prostanoids, an increased synthesis of nitric oxide, a reduced responsiveness of afferent glomerular arterioles to vasoconstrictor stimuli due to diabetic metabolic disturbances and a decreased receptor density for angiotensin II. It has been known for years that angiotensin II is formed locally due to the local activation of the renin angiotensin system. The local angiotensin II concentration, however, is not only regulated by the synthesis rate but also by the local degradation through activation of an aminopeptidase. The main finding of the present study was that the mRNA expression and activity of the angiotensin II degrading enzyme, angiotensinase A, was increased twofold in diabetic rats at 5 weeks and that the increase in mRNA expression was suppressed by insulin therapy and short-term treatment with the angiotensin II antagonist saralasin, whereas angiotensinase A enzyme activity was only reduced by saralasin and not by insulin. These results demonstrate that the angiotensin II degrading exopeptidase angiotensinase A is activated in diabetic glomeruli. This increased activity may be an additional mechanism to explain glomerular hyperfiltration and hyperperfusion in early diabetic nephropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418342
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Angiotensin converting-enzyme inhibitor treatment reduces glomerular p16INK4 and p27Kip1 expression in diabetic BBdp rats (1999)
    Springer
    Diabetologia 42 (1999), S. 1425-1432 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic nephropathy, cyclin-dependent kinase inhibitors, glomerular hypertrophy, cell cycle arrest, angiotensin II, progression of renal failure.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Renal hypertrophy occurs early in diabetes mellitus and precedes the development of glomerulosclerosis and tubulointerstitial fibrosis. We have previously shown that cultured mesangial cells exposed to high glucose are arrested in the G1-phase of the cell cycle and undergo cellular hypertrophy. High glucose-mediated induction of p27Kip1, an inhibitor of cyclin-dependent kinases, is essential in this process. Further investigations have also shown that p27Kip1 and p21Cip1, other cyclin-dependent kinase inhibitors, are up regulated in the kidneys of mice with Type I (insulin-dependent) as well as Type II (non-insulin-dependent) diabetes mellitus. Our study was undertaken to test a potential effect of short-term treatment with the angiotensin-converting enzyme inhibitor enalapril on the glomerular expression of the cyclin-dependent kinase inhibitors p16INK4, p21Cip1, and p27Kip1 in BBdp rats, an autoimmune model of Type I diabetes.¶Methods. We evaluated p16INK4, p21Cip1, and p27Kip1 protein expression in isolated glomeruli by western blots. We also assessed p27Kip1 positive glomerular cells by immunohistochemistry.¶Results. Glomerular expression of all three cyclin-dependent kinase inhibitors were stimulated in BBdp rats compared with non-diabetic BBdr animals. Enalapril treatment for 3 weeks, started after the onset of diabetes, reduced the glomerular expression of p16INK4 and p27Kip1 but not of p21Cip1. Enalapril also prevented the increase in kidney weights observed in BBdp rats but had no effect on systolic blood pressure or glucose concentrations.¶Conclusion/interpretation. Our data show that enalapril attenuates the glomerular expression of cyclin-dependent kinase inhibitors in diabetes and suggest a molecular mechanism of how angiotensin-converting enzyme inhibitors prevent renal hypertrophy in diabetes. [Diabetologia (1999) 42: 1425–1432]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051314
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Eine 73jährige Patientin mit hypertensiver Krise War der Einsatz des Kalziumantagonisten Nifedipin gerechtfertigt? (1999)
    Springer
    Der Internist 40 (1999), S. 205-209 
    Details
    ISSN: 1432-1289
    Keywords: Schlüsselwörter Nifedipin ; Kalziumantagonisten ; Koronare Herzkrankheit ; Hypertensive Krise ; Hypertensive Dringlichkeit ; Evidence Based Medicine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Zusammenfassung Eine 73jährige Patientin erwachte in der Nacht mit linksthorakalen Schmerzen und Herzklopfen. Der herbeigerufene Notarzt diagnostizierte eine hypertensive Krise. Der Blutdruck war 260/120 mm Hg, und der Notarzt verabreichte 50 mg Urapidil i.v.. Es folgte der Transport in die Klinik. In der Notaufnahme war der Blutdruck mit 190/120 mm Hg weiterhin erhöht. Die Patientin war beschwerdefrei. Das EKG zeigte keine Ischämie-typischen oder Infarkt-verdächtigen Veränderungen. Nach Gabe von 10 mg Nifedipin als Kapsel kam es zum schnellen Abfall des Blutdrucks auf 120/80 mm Hg. Es entwickelte sich eine Tachykardie, und heftige linksthorakale Schmerzen traten auf. Das EKG zeigte eine Sinustachykardie mit Ischämie-typischen ST-Streckensenkungen von 0.3 mV in den Brustwandableitungen. Die Symptomatik besserte sich nach i.v. Gabe von Nitroglycerin und Frequenzkontrolle. Das 12 h später geschriebene EKG zeigte keine Ischämie-typischen Veränderungen. Nach Intensivierung der antihypertensiven Therapie wurde die Patientin beschwerdefrei entlassen. Bei der Patientin waren durch die Gabe von Nifedipin Angina pectoris Beschwerden und ischämietypische EKG-Veränderungen ausgelöst worden. Wir diskutieren, warum wir trotz dieser Beobachtung den Gebrauch von Nifedipinkapseln bei der hypertensiven Krise für gerechtfertigt halten.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001080050325
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Akutes Nierenversagen Isolierte Manifestation einer Systemerkrankung (1997)
    Springer
    Der Internist 38 (1997), S. 606-609 
    Details
    ISSN: 1432-1289
    Keywords: Schlüsselwörter Sarkoidose ; Niereninsuffizienz ; Kalziumnephropathie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Zusammenfassung Eine Sarkoidose der Niere kann isoliert oder im Rahmen einer Systemerkrankung auftreten. Als diagnostisches Leitsymptom dient eine Nierenfunktionsverschlechterung, deren Ursache interstitielle Nephritiden, Glomerulonephritiden oder eine Kalziumnephropathie sein können. Eine Nierenbiopsie ist als wertvolles, differentialdiagnostisches Kriterium frühzeitig indiziert. Störungen des Kalziumstoffwechsels können ebenfalls diagnostisch wegweisend sein. Unter Therapie mit Steroiden kommt es in den meisten Fällen einer Sarkoidose der Niere zu einer guten Restitution der Nierenfunktion. Wesentlich ist, bei einer Niereninsuffizienz unklarer Ätiologie eine Sarkoidose in die differentialdiagnostischen Überlegungen einzubeziehen und frühzeitig mit einer adäquaten Therapie zu beginnen, um Spätschäden zu verhindern.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001080050073
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    Paper (German National Licenses)
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