ArticleThe Journal of physiology2006
Glucose reduces endothelin inhibition of voltage-gated potassium channels in rat arterial smooth muscle cells.
Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Arterial Myocyte Pannexin 1 Channel Controls Vascular Reactivity in Diabetic Hyperglycemia.Circulation research · 2025Article
- Spatiotemporal Control of Vascular CaCirculation research · 2022Article
- Selective protein kinase C inhibition switches time-dependent glucose cardiotoxicity to cardioprotection.Frontiers in cardiovascular medicine · 2022Article
- Lymphatic Collecting Vessel: New Perspectives on Mechanisms of Contractile Regulation and Potential Lymphatic Contractile Pathways to Target in Obesity and Metabolic Diseases.Frontiers in pharmacology · 2022Review
- Cellular and molecular effects of hyperglycemia on ion channels in vascular smooth muscle.Cellular and molecular life sciences : CMLS · 2021Review
- AKAP5 complex facilitates purinergic modulation of vascular L-type CaNature communications · 2020Article
- Adenylyl cyclase 5-generated cAMP controls cerebral vascular reactivity during diabetic hyperglycemia.The Journal of clinical investigation · 2019Article
- Evolving mechanisms of vascular smooth muscle contraction highlight key targets in vascular disease.Biochemical pharmacology · 2018Review
- Regulation of voltage-gated potassium channels in vascular smooth muscle during hypertension and metabolic disorders.Microcirculation (New York, N.Y. : 1994) · 2018Review
- KMicrocirculation (New York, N.Y. : 1994) · 2018Review
- Predominant contribution of L-type Cav1.2 channel stimulation to impaired intracellular calcium and cerebral artery vasoconstriction in diabetic hyperglycemia.Channels (Austin, Tex.) · 2017Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Ser1928 phosphorylation by PKA stimulates the L-type Ca2+ channel CaV1.2 and vasoconstriction during acute hyperglycemia and diabetes.Science signaling · 2017Article
- Protein Kinase C as Regulator of Vascular Smooth Muscle Function and Potential Target in Vascular Disorders.Advances in pharmacology (San Diego, Calif.) · 2017Review
- Distinct and complementary roles for α and β isoenzymes of PKC in mediating vasoconstrictor responses to acutely elevated glucose.British journal of pharmacology · 2016Article
- Selective down-regulation of KV2.1 function contributes to enhanced arterial tone during diabetes.The Journal of biological chemistry · 2015Article
- Ca2+ dependent but PKC independent signalling mediates UTP induced contraction of rat mesenteric arteries.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2015Article
- Article
- Cardiovascular impact of drugs used in the treatment of diabetes.Therapeutic advances in chronic disease · 2014 · on this mapReview
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Prolonged hyperglycaemia impairs vascular reactivity and inhibits voltage-activated K(+) (Kv) channels. We examined acute effects of altering glucose concentration on the activity and inhibition by endothelin-1 (ET-1) of Kv currents of freshly isolated rat arterial myocytes. Peak Kv currents recorded in glucose-free solution were reversibly reduced within 200 s by increasing extracellular glucose to 4 mm. This inhibitory effect of glucose was abolished by protein kinase C inhibitor peptide (PKC-IP), and Kv currents were further reduced in 10 mm glucose. In current-clamped cells, membrane potentials were more negative in 4 than in 10 mm glucose. In 4 mm d-glucose, 10 nm ET-1 decreased peak Kv current amplitude at +60 mV from 23.5 +/- 3.3 to 12.1 +/- 3.1 pA pF(-1) (n = 6, P < 0.001) and increased the rate of inactivation, decreasing the time constant around fourfold. Inhibition by ET-1 was prevented by PKC-IP. When d-glucose was increased to 10 mm, ET-1 no longer inhibited Kv current (n = 6). Glucose metabolism was required for prevention of ET-1 inhibition of Kv currents, since fructose mimicked the effects of d-glucose, while l-glucose, sucrose or mannitol were without effect. Endothelin receptors were still functional in 10 mm d-glucose, since pinacidil-activated ATP-dependent K(+) (K(ATP)) currents were reduced by 10 nm ET-1. This inhibition was nearly abolished by PKC-IP, indicating that endothelin receptors could still activate PKC in 10 mm d-glucose. These results indicate that changes in extracellular glucose concentration within the physiological range can reduce Kv current amplitude and can have major effects on Kv channel modulation by vasoconstrictors.
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