ArticleThe Journal of physiology1993
Membrane potential modulates inositol 1,4,5-trisphosphate-mediated Ca2+ transients in guinea-pig coronary myocytes.
Article in The Journal of physiology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 143 citations in OpenAlex.
- CaPhysiological reviews · 2024Review
- Engaging biological oscillators through second messenger pathways permits emergence of a robust gastric slow-wave during peristalsis.PLoS computational biology · 2021Article
- Calcium-Dependent Ion Channels and the Regulation of Arteriolar Myogenic Tone.Frontiers in physiology · 2021Review
- Introduction to ion channels and calcium signaling in the microcirculation.Current topics in membranes · 2020Review
- Spontaneous Electrical Activity and Rhythmicity in Gastrointestinal Smooth Muscles.Advances in experimental medicine and biology · 2019Review
- Voltage effects on muscarinic acetylcholine receptor-mediated contractions of airway smooth muscle.Physiological reports · 2018Article
- KMicrocirculation (New York, N.Y. : 1994) · 2018Review
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Potassium Channels in Regulation of Vascular Smooth Muscle Contraction and Growth.Advances in pharmacology (San Diego, Calif.) · 2017Review
- The significance of interstitial cells in neurogastroenterology.Journal of neurogastroenterology and motility · 2014Article
- ATP inhibits Ins(1,4,5)P3-evoked Ca2+ release in smooth muscle via P2Y1 receptors.Journal of cell science · 2012Article
- Direct voltage control of endogenous lysophosphatidic acid G-protein-coupled receptors in Xenopus oocytes.The Journal of physiology · 2010Article
- A Ca(2+)-activated Cl(-) conductance in interstitial cells of Cajal linked to slow wave currents and pacemaker activity.The Journal of physiology · 2009Article
- Upregulation of intermediate calcium-activated potassium channels counterbalance the impaired endothelium-dependent vasodilation in stroke-prone spontaneously hypertensive rats.Translational research : the journal of laboratory and clinical medicine · 2009Article
- High K+-induced contraction requires depolarization-induced Ca2+ release from internal stores in rat gut smooth muscle.Acta pharmacologica Sinica · 2009Article
- Mechanisms of oxygen sensing: a key to therapy of pulmonary hypertension and patent ductus arteriosus.British journal of pharmacology · 2008Review
- Changes in inward rectifier K+ channels in hepatic stellate cells during primary culture.Yonsei medical journal · 2008Article
- Novel consequences of voltage-dependence to G-protein-coupled P2Y1 receptors.British journal of pharmacology · 2008Article
- Effect of adenosine on membrane potential and Ca2+ in juxtaglomerular cells. Comparison with angiotensin II.Kidney & blood pressure research · 2008Article
- Factors modifying the frequency of spontaneous activity in gastric muscle.The Journal of physiology · 2006Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Vascular smooth muscle cells were isolated from the coronary artery of the guinea-pig. At 2.5 mM [Ca2+]o and 36 degrees C, whole cell membrane currents were recorded under voltage-clamp and the concentration of ionized calcium in the cytoplasm ([Ca2+]i) was monitored by indo-1 fluorescence. 2. At -60 mV, [Ca2+]i was 143 +/- 36 mM (mean +/- S.D.) and was insensitive to clamp steps to +100 mV. During 1 min application of acetylcholine (ACh, 10 microM) [Ca2+]i increased within approximately 2 s to 1480 +/- 250 nM. During the subsequent slow decay, [Ca2+]i was transiently increased by depolarizing clamp steps and decreased during hyperpolarizing steps. [Ca2+]i transients in response to caffeine (10 mM) could not be modulated by voltage steps. The results suggest that modulation of [Ca2+]i by membrane potential involves inositol 1,4,5-trisphosphate (Ins(1,4,5)P3)-induced Ca2+ release (IICR). 3. Modulation of IICR by membrane potential did not depend on sarcolemmal Ca2+ fluxes; it persisted after block of sarcolemmal Ca2+ fluxes with 3 mM lanthanum or after a change to nominally Ca(2+)-free bathing solutions. 4. Modulation of [Ca2+]i by membrane potential was recorded during cell dialysis of 50 microM GTP-gamma-S in the absence of ACh. Cell dialysis of exogenous Ins(1,4,5)P3 (50 or 100 microM) did not mimic the effects. The sensitivity of [Ca2+]i to depolarizing clamp steps was also induced by cell dialysis of lithium ions which, presumably, inhibited the breakdown of Ins(1,4,5)P3. The results are compatible with the idea that the membrane potential modulates the liberation of Ins(1,4,5)P3. 5. Modulation of IICR by membrane potential is discussed as a new mechanism that contributes to the regulation of activator calcium and to the modulation of contraction in vascular smooth muscle cells.
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