ArticleThe Journal of physiology1999
Dynamic Ca2+ signalling in rat arterial smooth muscle cells under the control of local renin-angiotensin system.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 35 citations in OpenAlex.
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- The cell-wide web coordinates cellular processes by directing site-specific CaNature communications · 2019Article
- Inositol trisphosphate receptors in smooth muscle cells.American journal of physiology. Heart and circulatory physiology · 2012Review
- Mechanism of asynchronous Ca(2+) waves underlying agonist-induced contraction in the rat basilar artery.British journal of pharmacology · 2009Article
- Mechanisms underlying angiotensin II-induced calcium oscillations.American journal of physiology. Renal physiology · 2008Article
- Smooth muscle sparklet Ca(v) channels defined: 1.2 is the number.American journal of physiology. Heart and circulatory physiology · 2007Article
- Angiotensin II-induced modulation of endothelium-dependent relaxation in rabbit mesenteric resistance arteries.The Journal of physiology · 2003Article
- The mechanism of phenylephrine-mediated [Ca(2+)](i) oscillations underlying tonic contraction in the rabbit inferior vena cava.The Journal of physiology · 2001Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. We visualized the changes in intracellular Ca2+ concentration ([Ca2+]i), using fluo-3 as an indicator, in individual smooth muscle cells within intact rat tail artery preparations. 2. On average in about 45 % of the vascular smooth muscle cells we found spontaneous Ca2+ waves and oscillations ( approximately 0.13 Hz), which we refer to here as Ca2+ ripples because the peak amplitude of [Ca2+]i was about one-seventh of that of Ca2+ oscillations evoked by noradrenaline. 3. We also found another pattern of spontaneous Ca2+ transients often in groups of two to three cells. They were rarely observed and are referred to as Ca2+ flashes because their peak amplitude was nearly twice as large as that in noradrenaline-evoked responses. 4. Sympathetic nerve activity was not considered responsible for the Ca2+ ripples, and they were abolished by inhibitors of either the Ca2+ pump in the sarcoplasmic reticulum (cyclopiazonic acid) or phospholipase C (U-73122). 5. Both angiotensin antagonists ([Sar1,Ile8]-angiotensin II and losartan) and an angiotensin converting enzyme inhibitor (captopril) inhibited the Ca2+ ripples. 6. The extracellular Ca2+-dependent tension borne by unstimulated arterial rings was reduced by the angiotensin antagonist by approximately 50 %. 7. These results indicate that the Ca2+ ripples are generated via inositol 1,4, 5-trisphosphate-induced Ca2+ release from the intracellular Ca2+ stores in response to locally produced angiotensin II, which contributes to the maintenance of vascular tone.
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