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  • 2000-2004  (2)
  • 1955-1959
  • D-serine  (1)
  • Key words Molecular genetics – DNA polymorphisms –¶angiotensinogen –¶angiotensin converting enzyme –¶genetic animal models  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Zeitschrift für Kardiologie 89 (2000), S. 264-268 
    ISSN: 1435-1285
    Keywords: Key words Molecular genetics – DNA polymorphisms –¶angiotensinogen –¶angiotensin converting enzyme –¶genetic animal models ; Schlüsselwörter Molekulargenetik – DNA-Polymorphismen –¶Angiotensinogen – Angiotensin-Converting Enzym –¶Genetische Tiermodelle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Seit der Entdeckung des Renins durch Tigerstedt und Bergmann ist das Renin-Angiotensin-System (RAS) als wichtiger Modulator von Blutdruck und Volumenhomöostase bekannt. Aufgrund dieser Wirkungen wurde dem RAS schon frühzeitig eine pathophysiologische Rolle bei Hypertonie und anderen kardiovaskulären Erkrankungen zugeschrieben. Der therapeutische Stellenwert der Hemmung des RAS durch den Einsatz von Angiotensin Converting-Enzym-(ACE)-Inhibitoren und AngiotensinII (AT1)-Rezeptorantagonisten ist unbestritten. Unklar ist allerdings, inwieweit die mit kardiovaskulären Erkrankungen einhergehenden Veränderungen in der Aktivität des RAS sekundäre und primäre Faktoren darstellen. Es ist bekannt, dass genetische Faktoren wesentlich zur Pathogenese der Hypertonie und ihrer Folgeerkrankungen beitragen. So wurden Genpolymorphismen für nahezu alle Komponenten des RAS beschrieben und in klinischen Studien untersucht. Offen ist jedoch vielfach die funktionelle Relevanz dieser Befunde. Im Folgenden soll daher versucht werden, insbesondere die genetischen Grundlagen einer kausalen Verknüpfung zwischen RAS und Pathogenese der kardiovaskulären Erkrankungen anhand aktueller Befunde zu diskutieren. Hierbei wird beispielhaft auf die Rolle von Angiotensinogen für die Hypertonie und Angiotensin Converting Enzym für Hypertonie, koronare Herzkrankheit und andere kardiovaskuläre Erkrankungen eingegangen.
    Notes: Summary Since the discovery of renin by Tigerstedt and Bergmann, the renin angiotensin system (RAS) has been recognized as an important modulator of blood pressure and volume homeostasis. Based on these functions a pathophysiological role of the RAS in the pathogenesis of hypertension and other cardiovascular disorders has been postulated. The therapeutic benefit of RAS inhibition by angiotensin converting enzyme (ACE) inhibitors and angiotensinII (ANGII) antagonists in these conditions has been shown. It remains unclear, however, whether the changes in RAS activity associated with cardiovascular disease are primary or secondary factors. It is well known that hypertension and hypertensive end-organ disease is influenced by genetic factors. Gene polymorphisms for virtually all components of the RAS have been described and investigated in clinical studies. It remains to be determined, however, how relevant these findings are for disease etiology. This review, therefore, will attempt to discuss the causal implications of these genetic studies for cardiovascular disease. The role of angiotensinogen and ACE for hypertension, coronary artery disease and other cardiovascular disorders is discussed in this context in an exemplary fashion.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Neurochemical research 25 (2000), S. 553-560 
    ISSN: 1573-6903
    Keywords: D-serine ; D-aspartate ; astrocytes ; N-methyl-D-aspartate (NMDA) receptor ; Bergmann glia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Of the twenty amino acids in the mammalian body, only serine and aspartate occur in D-configuration as well as L-configuration in significant amount. D-serine is selectively concentrated in the brain, localized to protoplasmic astrocytes that ensheath synapses and distributed similarly to N-methyl-D-aspartate (NMDA) subtype of glutamate receptors. D-serine has been found to function as an endogenous ligand for the “glycine” site of the NMDA receptor. Evidences for this include the greater potency of D-serine to activate this site than glycine, and D-amino acid oxidase, which degrades D-serine as well as other neutral D-amino acids, markedly attenuates NMDA neurotransmission. D-serine is also formed by serine racemase, a recently cloned enzyme that converts L-serine to D-serine. Thus, in many ways D-serine fulfills criteria for defining its functionality as a neurotransmitter and challenges the dogma relating to neurotransmission, for it is the “unnatural” isomeric form of an amino acid derived from glia rather than neurons.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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