The interaction of calcium entry and calcium sensitization in the control of vascular tone and blood pressure of normotensive and hypertensive rats
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem, přehledy
PubMed
24564658
DOI
10.33549/physiolres.932639
PII: 932639
Knihovny.cz E-zdroje
- MeSH
- gating iontového kanálu MeSH
- hypertenze patofyziologie MeSH
- krevní tlak * MeSH
- krysa rodu Rattus MeSH
- modely kardiovaskulární MeSH
- potkani inbrední SHR MeSH
- renin-angiotensin systém * MeSH
- rhoA protein vázající GTP metabolismus MeSH
- vápník metabolismus MeSH
- vápníková signalizace * MeSH
- vápníkové kanály metabolismus MeSH
- vazokonstrikce * MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- rhoA protein vázající GTP MeSH
- vápník MeSH
- vápníkové kanály MeSH
Increased systemic vascular resistance is responsible for blood pressure (BP) elevation in most forms of human or experimental hypertension. The enhanced contractility of structurally remodeled resistance arterioles is mediated by enhanced calcium entry (through L type voltage-dependent calcium channels - L-VDCC) and/or augmented calcium sensitization (mediated by RhoA/Rho kinase pathway). It is rather difficult to evaluate separately the role of these two pathways in BP control because BP response to the blockade of either pathway is always dependent on the concomitant activity of the complementary pathway. Moreover, vasoconstrictor systems enhance the activity of both pathways, while vasodilators attenuate them. The basal fasudil-sensitive calcium sensitization determined in rats deprived of endogenous renin-angiotensin system (RAS) and sympathetic nervous system (SNS) in which calcium entry was dose-dependently increased by L-VDCC opener BAY K8644, is smaller in spontaneously hypertensive rats (SHR) than in normotensive Wistar-Kyoto (WKY) rats. In contrast, if endogenous RAS and SNS were present in intact rats, fasudil caused a greater BP fall in SHR than WKY rats. Our in vivo experiments indicated that the endogenous pressor systems (RAS and SNS) augment calcium sensitization mediated by RhoA/Rho kinase pathway, whereas the endogenous vasodilator systems (such as nitric oxide) attenuate this pathway. However, the modulation of calcium entry and calcium sensitization by nitric oxide is strain-dependent because NO deficiency significantly augments low calcium entry in WKY and low calcium sensitization in SHR. Further in vivo and in vitro experiments should clarify the interrelationships between endogenous vasoactive systems and the contribution of calcium entry and/or calcium sensitization to BP maintenance in various forms of experimental hypertension.
Citace poskytuje Crossref.org
Altered Balance between Vasoconstrictor and Vasodilator Systems in Experimental Hypertension
