ArticleInvestigative ophthalmology & visual science2011
Endothelin 1 stimulates Ca2+-sparks and oscillations in retinal arteriolar myocytes via IP3R and RyR-dependent Ca2+ release.
Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Pulsed infrared releases CaJournal of neurophysiology · 2018Article
- Isolation of Retinal Arterioles for Ex Vivo Cell Physiology Studies.Journal of visualized experiments : JoVE · 2018Article
- Divergent signaling mechanisms for venous versus arterial contraction as revealed by endothelin-1.Journal of vascular surgery · 2015Article
- Ca(2+) sparks promote myogenic tone in retinal arterioles.British journal of pharmacology · 2013Article
- Automated region of interest analysis of dynamic Ca²+ signals in image sequences.American journal of physiology. Cell physiology · 2012Article
- Inositol trisphosphate receptors in smooth muscle cells.American journal of physiology. Heart and circulatory physiology · 2012Review
- Constriction of retinal arterioles to endothelin-1: requisite role of rho kinase independent of protein kinase C and L-type calcium channels.Investigative ophthalmology & visual science · 2012Article
- Feedback via Ca²⁺-activated ion channels modulates endothelin 1 signaling in retinal arteriolar smooth muscle.Investigative ophthalmology & visual science · 2012Article
- Function and expression of ryanodine receptors and inositol 1,4,5-trisphosphate receptors in smooth muscle cells of murine feed arteries and arterioles.The Journal of physiology · 2012Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
purposeTo investigate endothelin 1 (Et1)-dependent Ca(2+)-signaling at the cellular and subcellular levels in retinal arteriolar myocytes.
methodsEt1 responses were imaged from Fluo-4-loaded smooth muscle in isolated segments of rat retinal arteriole using confocal laser microscopy.
resultsBasal [Ca(2+)](i), subcellular Ca(2+)-sparks, and cellular Ca(2+)-oscillations were all increased during exposure to Et1 (10 nM). Ca(2+)-spark frequency was also increased by 90% by 10 nM Et1. The increase in oscillation frequency was concentration dependent and was inhibited by the EtA receptor (Et(A)R) blocker BQ123 but not by the EtB receptor antagonist BQ788. Stimulation of Ca(2+)-oscillations by Et1 was inhibited by a phospholipase C blocker (U73122; 10 μM), two inhibitors of inositol 1,4,5-trisphosphate receptors (IP(3)Rs), xestospongin C (10 μM), 2-aminoethoxydiphenyl borate (100 μM), and tetracaine (100 μM), a blocker of ryanodine receptors (RyRs).
conclusionsEt1 stimulates Ca(2+)-sparks and oscillations through Et(A)Rs. The underlying mechanism involves the activation of phospholipase C and both IP(3)Rs and RyRs, suggesting crosstalk between these Ca(2+)-release channels. These findings suggest that phasic Ca(2+)-oscillations play an important role in the smooth muscle response to Et1 within the retinal microvasculature and support an excitatory, proconstrictor role for Ca(2+)-sparks in these vessels.
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