ArticleThe Journal of physiology2001
The mechanism of phenylephrine-mediated [Ca(2+)](i) oscillations underlying tonic contraction in the rabbit inferior vena cava.
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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55 citing papers in PubMed, 166 citations in OpenAlex.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. We characterized the mechanisms in vascular smooth muscle cells (VSMCs) that produce asynchronous, wave-like Ca(2+) oscillations in response to phenylephrine (PE). Confocal imaging was used to observe [Ca(2+)](i) in individual VSMCs of intact inferior vena cava (IVC) from rabbits. 2. It was found that the Ca(2+) waves were initiated by Ca(2+) release from the sarcoplasmic reticulum (SR) via inositol 1,4,5-trisphosphate-sensitive SR Ca(2+) release channels (IP(3)R channels) and that refilling of the SR Ca(2+) store through the sarcoplasmic-endoplasmic reticulum Ca(2+)-ATPase (SERCA) was required for maintained generation of the repetitive Ca(2+) waves. 3. Blockade of L-type voltage-gated Ca(2+) channels (L-type VGCCs) with nifedipine reduced the frequency of PE-stimulated [Ca(2+)](i) oscillations, while additional blockade of receptor-operated channels/store-operated channels (ROCs/SOCs) with SKF96365 abolished the remaining oscillations. Parallel force measurements showed that nifedipine inhibited PE-induced tonic contraction by 27 % while SKF96365 abolished it. This indicates that stimulated Ca(2+) entry refills the SR to support the recurrent waves of SR Ca(2+) release and that both L-type VGCCs and ROCs/SOCs contribute to this process. 4. Application of the Na(+)-Ca(2+) exchanger (NCX) inhibitors 2',4'-dichlorobenzamil (forward- and reverse-mode inhibitor) and KB-R7943 (reverse-mode inhibitor) completely abolished the nifedipine-resistant component of [Ca(2+)](i) oscillations and markedly reduced PE-induced tone. 5. Thus, we conclude that each Ca(2+) wave depends on initial SR Ca(2+) release via IP(3)R channels followed by SR Ca(2+) refilling through SERCA. Na(+) entry through ROCs/SOCs facilitates Ca(2+) entry through the NCX operating in the reverse mode, which refills the SR and maintains PE-induced [Ca(2+)](i) oscillations. In addition some Ca(2+) entry through L-type VGCCs and ROCs/SOCs serves to modulate the frequency of the oscillations and the magnitude of force development.
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