Ontogenetic changes in contribution of calcium sensitization and calcium entry to blood pressure maintenance of Wistar-Kyoto and spontaneously hypertensive rats
Jazyk angličtina Země Nizozemsko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
- MeSH
- 1-(5-isochinolinsulfonyl)-2-methylpiperazin analogy a deriváty farmakologie MeSH
- arterie účinky léků patofyziologie MeSH
- blokátory kalciových kanálů farmakologie MeSH
- exprese genu účinky léků MeSH
- faktory zaměňující Rho guanin nukleotidy genetika MeSH
- fosfoproteiny genetika metabolismus MeSH
- fosforylace MeSH
- hypertenze patofyziologie MeSH
- inhibitory proteinkinas farmakologie MeSH
- kinázy asociované s rho antagonisté a inhibitory metabolismus MeSH
- krevní tlak účinky léků fyziologie MeSH
- krysa rodu Rattus MeSH
- messenger RNA metabolismus MeSH
- nifedipin farmakologie MeSH
- potkani inbrední SHR MeSH
- potkani inbrední WKY MeSH
- rhoA protein vázající GTP metabolismus MeSH
- signální transdukce MeSH
- svalová kontrakce MeSH
- svalové proteiny genetika metabolismus MeSH
- svaly hladké cévní účinky léků fyziologie MeSH
- vápník metabolismus MeSH
- vápníkové kanály - typ L účinky léků metabolismus MeSH
- výměnné faktory guaninnukleotidů genetika 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
- 1-(5-isochinolinsulfonyl)-2-methylpiperazin MeSH
- Arhgef11 protein, rat MeSH Prohlížeč
- Arhgef12 protein, rat MeSH Prohlížeč
- blokátory kalciových kanálů MeSH
- faktory zaměňující Rho guanin nukleotidy MeSH
- fasudil MeSH Prohlížeč
- fosfoproteiny MeSH
- inhibitory proteinkinas MeSH
- kinázy asociované s rho MeSH
- messenger RNA MeSH
- nifedipin MeSH
- p63RhoGEF protein, rat MeSH Prohlížeč
- Ppp1r14a protein, rat MeSH Prohlížeč
- rhoA protein vázající GTP MeSH
- svalové proteiny MeSH
- vápník MeSH
- vápníkové kanály - typ L MeSH
- výměnné faktory guaninnukleotidů MeSH
BACKGROUND: Altered calcium sensitization (mediated by RhoA/Rho-kinase pathway) and enhanced calcium entry through L-type voltage-dependent calcium channels (L-VDCCs) participate in blood pressure (BP) maintenance of adult spontaneously hypertensive rats (SHRs). This study aimed to evaluate ontogenetic changes of these two pathways in BP control of SHR and Wistar-Kyoto (WKY) aged 3, 5, 7, 13, 26 and 42 weeks. METHODS: BP response to acute administration of Rho-kinase inhibitor fasudil or L-VDCC blocker nifedipine and the expression of particular components of RhoA/Rho-kinase pathway were determined in young and adult animals. RESULTS: Fasudil-induced BP reduction was attenuated in young SHR compared with WKY, but was enhanced in adult SHR. In contrast, BP response to nifedipine was similar in 3-week-old SHR and WKY and it was augmented with age in SHR but not in WKY. Consequently, the ratio between fasudil-induced and nifedipine-induced BP changes was lower in all age groups of SHR compared with WKY. Fasudil effects on contractility of isolated arteries were attenuated in young but not in adult SHR. mRNA expression of selected Rho-GEFs (Arhgef1, Arhgef11 and Arhgef12) was decreased only in adult SHR, whereas p63RhoGEF and CPI-17 expression was reduced in both age groups of SHR. Active RhoA and phosphorylated CPI-17 were increased in adult but not in young SHR. CONCLUSION: The importance of RhoA/Rho-kinase pathway for BP/vascular tone control is attenuated in SHR from prehypertensive stages. Enhanced RhoA activation and/or CPI-17 phosphorylation might be counteracted by reduced expression of upstream activators of Rho-kinase (Rho-GEFs) together with lower expression of CPI-17 (in downstream cascade of Rho-kinase).
Citace poskytuje Crossref.org
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