ArticleAmerican journal of physiology. Heart and circulatory physiology2014
KIR channel activation contributes to onset and steady-state exercise hyperemia in humans.
Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 40 citations in OpenAlex.
- Amplification of endothelium-dependent vasodilatation in contracting human skeletal muscle: role of KThe Journal of physiology · 2019Trial
- Prolonged adenosine triphosphate infusion and exercise hyperemia in humans.Journal of applied physiology (Bethesda, Md. : 1985) · 2016Trial
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- The Emerging Role of Endothelial Ion Channels in the Control of Human Microcirculation.International journal of molecular sciences · 2026Review
- Compensatory Oxygenation Changes in Non-active and Active Muscles During Incremental Exercise in Healthy Adults.Advances in experimental medicine and biology · 2026Article
- Global REACH 2018: increased adrenergic restraint of blood flow preserves coupling of oxygen delivery and demand during exercise at high-altitude.The Journal of physiology · 2022Article
- Endothelial Ion Channels and Cell-Cell Communication in the Microcirculation.Frontiers in physiology · 2022Review
- Impairment of Flow-Sensitive Inwardly Rectifying KArteriosclerosis, thrombosis, and vascular biology · 2020Article
- KThe Journal of physiology · 2020Article
- Assessment of resistance vessel function in human skeletal muscle: guidelines for experimental design, Doppler ultrasound, and pharmacology.American journal of physiology. Heart and circulatory physiology · 2020Review
- Sustained exercise hyperemia during prolonged adenosine infusion in humans.Physiological reports · 2019Article
- Inhibition of NaThe Journal of physiology · 2018Article
- Elevated extracellular potassium prior to muscle contraction reduces onset and steady-state exercise hyperemia in humans.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- Capillary response to skeletal muscle contraction: evidence that redundancy between vasodilators is physiologically relevant during active hyperaemia.The Journal of physiology · 2018Article
- Phosphodiesterase-5 inhibition preserves exercise-onset vasodilator kinetics when NOS activity is reduced.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- Microvascular Vasodilator Plasticity After Acute Exercise.Exercise and sport sciences reviews · 2018Review
- Rapid versus slow ascending vasodilatation: intercellular conduction versus flow-mediated signalling with tetanic versus rhythmic muscle contractions.The Journal of physiology · 2017Article
- Skeletal muscle contraction-induced vasodilation in the microcirculation.Journal of exercise rehabilitation · 2017Review
- Sympatholytic effect of intravascular ATP is independent of nitric oxide, prostaglandins, NaThe Journal of physiology · 2017Article
- Increased amplitude of inward rectifier KAmerican journal of physiology. Heart and circulatory physiology · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
We tested the hypothesis that activation of inwardly rectifying potassium (KIR) channels and Na(+)-K(+)-ATPase, two pathways that lead to hyperpolarization of vascular cells, contributes to both the onset and steady-state hyperemic response to exercise. We also determined whether after inhibiting these pathways nitric oxide (NO) and prostaglandins (PGs) are involved in the hyperemic response. Forearm blood flow (FBF; Doppler ultrasound) was determined during rhythmic handgrip exercise at 10% maximal voluntary contraction for 5 min in the following conditions: control [saline; trial 1 (T1)]; with combined inhibition of KIR channels and Na(+)-K(+)-ATPase alone [via barium chloride (BaCl2) and ouabain, respectively; trial 2 (T2)]; and with additional combined nitric oxide synthase (N(G)-monomethyl-l-arginine) and cyclooxygenase inhibition [ketorolac; trial 3 (T3)]. In T2, the total hyperemic responses were attenuated ~50% from control (P < 0.05) at exercise onset, and there was minimal further effect in T3 (protocol 1; n = 11). In protocol 2 (n = 8), steady-state FBF was significantly reduced during T2 vs. T1 (133 ± 15 vs. 167 ± 17 ml/min; Δ from control: -20 ± 3%; P < 0.05) and further reduced during T3 (120 ± 15 ml/min; -29 ± 3%; P < 0.05 vs. T2). In protocol 3 (n = 8), BaCl2 alone reduced FBF during onset (~50%) and steady-state exercise (~30%) as observed in protocols 1 and 2, respectively, and addition of ouabain had no further impact. Our data implicate activation of KIR channels as a novel contributing pathway to exercise hyperemia in humans.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.