ArticleThe Journal of physiology1999
Substance P and bradykinin activate different types of KCa currents to hyperpolarize cultured porcine coronary artery endothelial cells.
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 21 papers.
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Who cites it
21 citing papers in PubMed, 61 citations in OpenAlex.
- Oxidative and Nitrous Stress Underlies Vascular Malfunction Induced by Ionizing Radiation and Diabetes.Cardiovascular toxicology · 2024Review
- Differential hyperpolarization to substance P and calcitonin gene-related peptide in smooth muscle versus endothelium of mouse mesenteric artery.Microcirculation (New York, N.Y. : 1994) · 2021Article
- Overview of Antagonists Used for Determining the Mechanisms of Action Employed by Potential Vasodilators with Their Suggested Signaling Pathways.Molecules (Basel, Switzerland) · 2016Review
- Muscle KATP channels: recent insights to energy sensing and myoprotection.Physiological reviews · 2010Review
- Differential regulation of calcium-activated potassium channels by dynamic intracellular calcium signals.The Journal of membrane biology · 2010Article
- Adenosine receptors and the heart: role in regulation of coronary blood flow and cardiac electrophysiology.Handbook of experimental pharmacology · 2009Review
- Kaempferol stimulates large conductance Ca2+ -activated K+ (BKCa) channels in human umbilical vein endothelial cells via a cAMP/PKA-dependent pathway.British journal of pharmacology · 2008Article
- The cellular mechanisms by which adenosine evokes release of nitric oxide from rat aortic endothelium.The Journal of physiology · 2006Article
- Twenty years of calcium imaging: cell physiology to dye for.Molecular interventions · 2005Review
- Endothelium-dependent smooth muscle hyperpolarization: do gap junctions provide a unifying hypothesis?British journal of pharmacology · 2004Review
- Anandamide initiates Ca(2+) signaling via CB2 receptor linked to phospholipase C in calf pulmonary endothelial cells.British journal of pharmacology · 2003Article
- Modelling the electrophysiological endothelial cell response to bradykinin.European biophysics journal : EBJ · 2003Article
- Characterization of a charybdotoxin-sensitive intermediate conductance Ca2+-activated K+ channel in porcine coronary endothelium: relevance to EDHF.British journal of pharmacology · 2002Article
- Charybdotoxin-sensitive small conductance K(Ca) channel activated by bradykinin and substance P in endothelial cells.British journal of pharmacology · 2002Article
- Subplasmalemmal endoplasmic reticulum controls K(Ca) channel activity upon stimulation with a moderate histamine concentration in a human umbilical vein endothelial cell line.The Journal of physiology · 2002Article
- Characterization of an apamin-sensitive small-conductance Ca(2+)-activated K(+) channel in porcine coronary artery endothelium: relevance to EDHF.British journal of pharmacology · 2002Article
- Further investigations into the endothelium-dependent hyperpolarizing effects of bradykinin and substance P in porcine coronary artery.British journal of pharmacology · 2001Article
- An evaluation of potassium ions as endothelium-derived hyperpolarizing factor in porcine coronary arteries.British journal of pharmacology · 2000Article
- ATP-sensitive potassium channels in capillaries isolated from guinea-pig heart.The Journal of physiology · 2000Article
- Subplasmalemmal ryanodine-sensitive Ca2+ release contributes to Ca2+-dependent K+ channel activation in a human umbilical vein endothelial cell line.The Journal of physiology · 2000Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Substance P and bradykinin, endothelium-dependent vasodilators of pig coronary artery, trigger in endothelial cells a rise in cytosolic Ca2+ concentration ([Ca2+]i) and membrane hyperpolarization. The aim of the present study was to determine the type of Ca2+-dependent K+ (KCa) currents underlying the endothelial cell hyperpolarization. 2. The substance P-induced increase in [Ca2+]i was 30 % smaller than that induced by bradykinin, although the two peptides triggered a membrane hyperpolarization of the same amplitude. The two agonists evoked a large outward K+ current of the same conductance at maximal stimulation. Agonists applied together produced the same maximal current amplitude as either one applied alone. 3. Iberiotoxin (50 nM) reduced by about 40 % the K+ current activated by bradykinin without modifying the substance P response. Conversely, apamin (1 microM) inhibited the substance P-induced K+ current by about 65 %, without affecting the bradykinin response. Similar results were obtained on peptide-induced membrane hyperpolarization. 4. Bradykinin-induced, but not substance P-induced, endothelium-dependent relaxation resistant to NG-nitro-L-arginine and indomethacin was partly inhibited by 3 microM 17-octadecynoic acid (17-ODYA), an inhibitor of cytochrome P450 epoxygenase. Similarly, the bradykinin-induced K+ current was reduced by 17-ODYA. 5. Our results show that responses to substance P and bradykinin result in a hyperpolarization due to activation of different KCa currents. A current consistent with the activation of large conductance (BKCa) channels was activated only by bradykinin, whereas a current consistent with the activation of small conductance (SKCa) channels was stimulated only by substance P. The observation that a similar electrical response is produced by different pools of channels implies distinct intracellular pathways leading to KCa current activation.
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