ArticlePflugers Archiv : European journal of physiology2007
Ketamine blocks voltage-gated K(+) channels and causes membrane depolarization in rat mesenteric artery myocytes.
Article in Pflugers Archiv : European journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Adverse Effects Associated With High-Dose Ketamine Infusions For Refractory Pain And Psychiatric Conditions.Current pain and headache reports · 2025Review
- The involvement of KTranslational psychiatry · 2024Review
- Spike firing attenuation of serotonin neurons in learned helplessness rats is reversed by ketamine.Brain communications · 2021Article
- Fluid flow facilitates inward rectifier KScientific reports · 2016Article
- Facilitation of serotonin-induced contraction of rat mesenteric artery by ketamine.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016Article
- Hydrogen peroxide induces vasorelaxation by enhancing 4-aminopyridine-sensitive Kv currents through S-glutathionylation.Pflugers Archiv : European journal of physiology · 2015Article
- Serotonin contracts the rat mesenteric artery by inhibiting 4-aminopyridine-sensitive Kv channels via the 5-HT2A receptor and Src tyrosine kinase.Experimental & molecular medicine · 2013Article
- Vasorelaxant mechanisms of ketamine in rabbit renal artery.Korean journal of anesthesiology · 2012Article
- Astrocytic calcium signaling: the information currency coupling neuronal activity to the cerebral microcirculation.Trends in cardiovascular medicine · 2007Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clinical doses of ketamine typically increase blood pressure, heart rate, and cardiac output. However, the precise mechanism by which ketamine produces these cardiovascular effects remains unclear. The voltage-gated K(+) (K(V)) channel is the major regulator of resting membrane potential (E (m)) and vascular tone in many arteries. Therefore, we sought to evaluate the effects of ketamine on K(V) currents using the standard whole-cell patch clamp recordings in single myocytes, enzymatically dispersed from rat mesenteric arteries. Ketamine [(+/-)-racemic mixture] inhibited K(V) currents reversibly and concentration dependently with a K ( d ) of 566.7 +/- 32.3 microM and Hill coefficient of 0.75 +/- 0.03. The inhibition of K(V) currents by ketamine was voltage independent, and the time courses of channel activation and inactivation were little affected. The effects of ketamine on steady-state activation and inactivation curves were also minimal. Use-dependent inhibition was not observed either. S(+)-ketamine inhibited K(V) currents with similar potency and efficacy as the racemic mixture. The average resting E (m) in rat mesenteric artery myocytes was -44.1 +/- 4.2 mV, and both racemic and S(+)-ketamine induced depolarization of E (m) (15.8 +/- 3.6 and 24.3 +/- 5.0 mV at 100 microM, respectively). We conclude that ketamine induces E (m) depolarization in vascular myocytes by blocking K(V) channels in a state-independent manner, which may contribute to the increased vascular tone and blood pressure produced by this drug under a clinical setting.
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