Renal interactions of renin-angiotensin system, nitric oxide and superoxide anion: implications in the pathophysiology of salt-sensitivity and hypertension
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem, přehledy
PubMed
20131937
DOI
10.33549/physiolres.931917
PII: 931917
Knihovny.cz E-zdroje
- MeSH
- angiotensin II metabolismus MeSH
- hypertenze etiologie metabolismus patofyziologie MeSH
- krevní tlak * MeSH
- kuchyňská sůl škodlivé účinky MeSH
- ledviny metabolismus patofyziologie MeSH
- lidé MeSH
- modely nemocí na zvířatech MeSH
- oxid dusnatý metabolismus MeSH
- oxidační stres * MeSH
- renin-angiotensin systém * MeSH
- sodík metabolismus MeSH
- superoxidy metabolismus MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- angiotensin II MeSH
- kuchyňská sůl MeSH
- oxid dusnatý MeSH
- sodík MeSH
- superoxidy MeSH
Renin-angiotensin system (RAS) plays a key role in the regulation of renal function, volume of extracellular fluid and blood pressure. The activation of RAS also induces oxidative stress, particularly superoxide anion (O(2)(-)) formation. Although the involvement of O(2)(-) production in the pathology of many diseases is known for long, recent studies also strongly suggest its physiological regulatory function of many organs including the kidney. However, a marked accumulation of O(2)(-) in the kidney alters normal regulation of renal function and thus may contribute to the development of salt-sensitivity and hypertension. In the kidney, O(2)(-) acts as vasoconstrictor and enhances tubular sodium reabsorption. Nitric oxide (NO), another important radical that exhibits opposite effects than O(2)(-), is also involved in the regulation of kidney function. O(2)(-) rapidly interacts with NO and thus, when O(2)(-) production increases, it diminishes the bioavailability of NO leading to the impairment of organ function. As the activation of RAS, particularly the enhanced production of angiotensin II, can induce both O(2)(-) and NO generation, it has been suggested that physiological interactions of RAS, NO and O(2)(-) provide a coordinated regulation of kidney function. The imbalance of these interactions is critically linked to the pathophysiology of salt-sensitivity and hypertension.
Citace poskytuje Crossref.org
Research on Experimental Hypertension in Prague (1966-2009)
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