ArticleVascular pharmacology
Caffeine inhibits InsP3 responses and capacitative calcium entry in canine pulmonary arterial smooth muscle cells.
Article in Vascular pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Pre-Exercise Caffeine as a Modulator of Exercise-Induced Acute Cardiometabolic Responses: A Narrative Review.Metabolites · 2026Review
- Neuronal regulation of myenteric interstitial cells of Cajal (ICC-MY) in the proximal colon.Cell calcium · 2025Article
- Ca²⁺ signaling in myenteric interstitial cells of Cajal (ICC-MY) and their role as conditional pacemakers in the colon.Cell calcium · 2025Article
- Long-Term Hypoxia Negatively Influences CaFrontiers in physiology · 2021Article
- A co-association network analysis of the genetic determination of pig conformation, growth and fatness.PloS one · 2014Article
- Prenatal programming of pulmonary hypertension induced by chronic hypoxia or ductal ligation in sheep.Pulmonary circulation · 2013Review
- Inhibition of parathyroid hormone secretion by caffeine in human parathyroid cells.The Journal of clinical endocrinology and metabolism · 2013Article
- Maternal high-altitude hypoxia and suppression of ryanodine receptor-mediated Ca2+ sparks in fetal sheep pulmonary arterial myocytes.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Alteration of Ryanodine-receptors in Cultured Rat Aortic Smooth Muscle Cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2011Article
- Article
- Mice null for calsequestrin 1 exhibit deficits in functional performance and sarcoplasmic reticulum calcium handling.PloS one · 2011Article
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Authors and funding
3 authors at 2 institutions in 1 country.
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Abstract
Caffeine is a well described and characterized ryanodine receptor (RyR) activator. Previous evidence from independent research studies also indicate caffeine inhibits InsP3 receptor functionality, which is important to activation of capacitative Ca2+ entry (CCE) in some cell types. In addition, RyR activation elicits excitatory-coupled Ca2+ entry (ECCE) in skeletal muscle myotubes. Recent studies by our group show that canine pulmonary arterial smooth muscle cells (PASMCs) have functional InsP3 receptors as well as RyRs, and that CCE is dependent on InsP3 receptor activity. The potential for caffeine to activate ECCE as well as inhibit InsP3 receptor function and CCE was examined using fura-2 fluorescent imaging in canine PASMCs. The data show caffeine causes transient as well as sustained cytosolic Ca2+ increases, though this is not due to CCE or ECCE activity as evidenced by a lack of an increase in Mn2+ quench of fura-2. The experiments also show caffeine reversibly inhibits 5-HT elicited-InsP3 mediated Ca2+ responses with an IC50 of 6.87x10(-4) M and 10 mM caffeine fully inhibits CCE. These studies provide the first evidence that caffeine is an inhibitor of InsP3 generated Ca2+ signals and CCE in PASMCs.
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