ArticleThe Journal of physiology1999
Contribution of Ca2+-activated K+ channels and non-selective cation channels to membrane potential of pulmonary arterial smooth muscle cells of the rabbit.
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 33 papers.
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Who cites it
33 citing papers in PubMed, 84 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Arterial NALCN Knockdown Ameliorates Mineralocorticoid-Induced Hypertension and Arterial Overcontractility.Circulation research · 2025Article
- Article
- A computational model predicts sex-specific responses to calcium channel blockers in mammalian mesenteric vascular smooth muscle.bioRxiv : the preprint server for biology · 2024Article
- Modulation of the Cardiac Myocyte Action Potential by the Magnesium-Sensitive TRPM6 and TRPM7-like Current.International journal of molecular sciences · 2021Article
- Article
- Maintenance of intracellular Ca2+ basal concentration in airway smooth muscle (Review).International journal of molecular medicine · 2018Review
- TbIRK is a signature sequence free potassium channel from Trypanosoma brucei locating to acidocalcisomes.Scientific reports · 2017Article
- Hydrogen peroxide induces vasorelaxation by enhancing 4-aminopyridine-sensitive Kv currents through S-glutathionylation.Pflugers Archiv : European journal of physiology · 2015Article
- Diverse Kir expression contributes to distinct bimodal distribution of resting potentials and vasotone responses of arterioles.PloS one · 2015Article
- Article
- Molecular and electrophysiological characterization of a novel cation channel of Trypanosoma cruzi.PLoS pathogens · 2012Article
- Hypoxic pulmonary vasoconstriction.Physiological reviews · 2012Review
- Basally activated nonselective cation currents regulate the resting membrane potential in human and monkey colonic smooth muscle.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- Molecular expression and functional role of canonical transient receptor potential channels in airway smooth muscle cells.Advances in experimental medicine and biology · 2011Review
- Functional role of canonical transient receptor potential 1 and canonical transient receptor potential 3 in normal and asthmatic airway smooth muscle cells.American journal of respiratory cell and molecular biology · 2010Article
- Knockdown of stromal interaction molecule 1 attenuates store-operated Ca2+ entry and Ca2+ responses to acute hypoxia in pulmonary arterial smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2009Article
- Store-operated calcium entry in vascular smooth muscle.British journal of pharmacology · 2008Review
- Ketamine blocks voltage-gated K(+) channels and causes membrane depolarization in rat mesenteric artery myocytes.Pflugers Archiv : European journal of physiology · 2007Article
- Signal transduction pathways and gating mechanisms of native TRP-like cation channels in vascular myocytes.The Journal of physiology · 2006Review
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. Using the perforated patch-clamp or whole-cell clamp technique, we investigated the contribution of Ca2+-activated K+ current (IK(Ca)) and non-selective cation currents (INSC) to the membrane potential in small pulmonary arterial smooth muscle cells of the rabbit. 2. The resting membrane potential (Vm) was -39.2 +/- 0.9 mV (n = 72). It did not stay at a constant level, but hyperpolarized irregularly, showing spontaneous transient hyperpolarizations (STHPs). The mean frequency and amplitude of the STHPs was 5.6 +/- 1. 1 Hz and -7.7 +/- 0.7 mV (n = 12), respectively. In the voltage-clamp mode, spontaneous transient outward currents (STOCs) were recorded with similar frequency and irregularity. 3. Intracellular application of BAPTA or extracellular application of TEA or charybdotoxin suppressed both the STHPs and STOCs. The depletion of intracellular Ca2+ stores by caffeine or ryanodine, and the removal of extracellular Ca2+ also abolished STHPs and STOCs. 4. Replacement of extracellular Na+ with NMDG+ caused hyperpolarization Vm of without affecting STHPs. Removal of extracellular Ca2+ induced a marked depolarization of Vm along with the disappearance of STHPs. 5. The ionic nature of the background inward current was identified. The permeability ratio of K+ : Cs+ : Na+ : Li+ was 1.7 : 1.3 : 1 : 0. 9, indicating that it is a non-selective cation current (INSC). The reversal potential of this current in control conditions was calculated to be -13.9 mV. The current was blocked by millimolar concentrations of extracellular Ca2+ and Mg2+. 6. From these results, it was concluded that (i) hyperpolarizing currents are mainly contributed by Ca2+-activated K+ (KCa) channels, and thus STOCs result in transient membrane hyperpolarization, and (ii) depolarizing currents are carried through NSC channels.
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