Captopril partially decreases the effect of H(2)S on rat blood pressure and inhibits H(2)S-induced nitric oxide release from S-nitrosoglutathione
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
25470515
DOI
10.33549/physiolres.932772
PII: 932772
Knihovny.cz E-zdroje
- MeSH
- antagonismus léků MeSH
- dechová frekvence fyziologie účinky záření MeSH
- kaptopril aplikace a dávkování MeSH
- krevní tlak účinky léků fyziologie MeSH
- krysa rodu Rattus MeSH
- lékové interakce MeSH
- oxid dusnatý metabolismus MeSH
- potkani Wistar MeSH
- S-nitrosoglutathion metabolismus MeSH
- sulfan metabolismus MeSH
- sulfidy aplikace a dávkování MeSH
- vztah mezi dávkou a účinkem léčiva MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- kaptopril MeSH
- oxid dusnatý MeSH
- S-nitrosoglutathion MeSH
- sodium sulfide MeSH Prohlížeč
- sulfan MeSH
- sulfidy MeSH
We studied the effects of the H(2)S donor Na(2)S on the mean arterial blood pressure (MAP) and heart and breathing rates of anesthetized Wistar rats in the presence and absence of captopril. Bolus administration of Na(2)S (1-4 micromol/kg) into the right jugular vein transiently decreased heart and increased breathing rates; at 8-30 micromol/kg, Na(2)S had a biphasic effect, transiently decreasing and increasing MAP, while transiently decreasing heart rate and increasing and decreasing breathing rate. These results may indicate independent mechanisms by which H(2)S influences MAP and heart and breathing rates. The effect of Na(2)S in decreasing MAP was less pronounced in the presence of captopril (2 micromol/l), which may indicate that the renin-angiotensin system is partially involved in the Na(2)S effect. Captopril decreased H(2)S-induced NO release from S-nitrosoglutathione, which may be related to some biological activities of H(2)S. These results contribute to the understanding of the effects of H(2)S on the cardiovascular system.
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