Acute and chronic role of nitric oxide, renin-angiotensin system and sympathetic nervous system in the modulation of calcium sensitization in Wistar rats
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
26291725
DOI
10.33549/physiolres.933094
PII: 933094
Knihovny.cz E-zdroje
- MeSH
- cévní rezistence fyziologie MeSH
- fyziologická adaptace fyziologie MeSH
- krevní tlak fyziologie MeSH
- krysa rodu Rattus MeSH
- kyselina dusičná metabolismus MeSH
- potkani Wistar MeSH
- renin-angiotensin systém fyziologie MeSH
- sympatický nervový systém fyziologie MeSH
- vápník metabolismus MeSH
- vazokonstrikce fyziologie 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
- kyselina dusičná MeSH
- vápník MeSH
Principal vasoactive systems - renin-angiotensin system (RAS), sympathetic nervous system (SNS), nitric oxide (NO) and prostanoids - exert their vascular effects through the changes in calcium levels and/or calcium sensitization. To estimate a possible modulation of calcium sensitization by the above vasoactive systems, we studied the influence of acute and chronic blockade of particular vasoactive systems on blood pressure (BP) changes elicited in conscious normotensive rats by acute dose-dependent administration of Rho-kinase inhibitor fasudil. Adult male chronically cannulated Wistar rats were used throughout this study. The acute inhibition of NO synthase (NOS) by L-NAME enhanced BP response to fasudil, the effect being considerably augmented in rats deprived of endogenous SNS. The acute inhibition of prostanoid synthesis by indomethacin modified BP response to fasudil less than the acute NOS inhibition. The chronic NOS inhibition caused moderate BP elevation and a more pronounced augmentation of fasudil-induced BP changes compared to the effect of acute NOS inhibition. This indicates both short-term and long-term NO-dependent attenuation of calcium sensitization. Long-term inhibition of RAS by captopril caused a significant attenuation of BP changes elicited by fasudil. In contrast, a long-term attenuation of SNS by chronic guanethidine treatment (in youth or adulthood) had no effect on BP response to fasudil, suggesting the absence of SNS does not affect calcium sensitization in vascular smooth muscle of normotensive rats. In conclusion, renin-angiotensin system contributes to the long-term increase of calcium sensitization and its effect is counterbalanced by nitric oxide which decreases calcium sensitization in Wistar rats.
Citace poskytuje Crossref.org
Altered Balance between Vasoconstrictor and Vasodilator Systems in Experimental Hypertension
