November 1993
Volume 34, Issue 12
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Articles  |   November 1993
Insulin-induced hyperpolarization in retinal capillary pericytes.
Author Affiliations
  • S Berweck
    Department of Clinical Physiology, Universitatsklinikum Steglitz, Freie Universität Berlin, Germany.
  • H Thieme
    Department of Clinical Physiology, Universitatsklinikum Steglitz, Freie Universität Berlin, Germany.
  • A Lepple-Wienhues
    Department of Clinical Physiology, Universitatsklinikum Steglitz, Freie Universität Berlin, Germany.
  • H Helbig
    Department of Clinical Physiology, Universitatsklinikum Steglitz, Freie Universität Berlin, Germany.
  • M Wiederholt
    Department of Clinical Physiology, Universitatsklinikum Steglitz, Freie Universität Berlin, Germany.
Investigative Ophthalmology & Visual Science November 1993, Vol.34, 3402-3407. doi:
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      S Berweck, H Thieme, A Lepple-Wienhues, H Helbig, M Wiederholt; Insulin-induced hyperpolarization in retinal capillary pericytes.. Invest. Ophthalmol. Vis. Sci. 1993;34(12):3402-3407.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

PURPOSE: This study investigated the mechanism of insulin-induced membrane voltage hyperpolarization in retinal capillary pericytes, which possess electrical membrane properties typical for smooth muscle cells and are supposed to regulate retinal microcirculation by a contractile mechanism. METHODS: The mechanism of insulin-induced hyperpolarization was studied in cultured bovine retinal capillary pericytes using conventional microelectrodes. RESULTS: Resting voltage averaged -28 +/- 0.9 mV (mean +/- SEM, n = 45). Insulin (10(-9) to 10(-7) mol/l) induced a slow hyperpolarization in a dose-dependent fashion. Voltage change (delta V) was -3.1 +/- 0.4 mV (n = 14, P < 0.0001, = control) with an insulin concentration of 10(-8) mol/l. Blockade of potassium channels with Ba2+ (5 mmol/l) completely abolished the hyperpolarizing effect of insulin (n = 5). Apamin (10(-9) mol/l), a blocker of low-conductance Ca(2+)-activated potassium channels, also completely inhibited the insulin-induced hyperpolarization (n = 4). Blocking ATP-sensitive potassium channels with glibenclamide (10(-7) mol/l) did not reduce the hyperpolarizing action of insulin (delta V = -2.2 +/- 0.4 mV, n = 5, P = 0.29). Equivalent hyperpolarizations were recorded when insulin was added in the presence of ouabain (10(-4) mol/l) to inhibit the electrogenic Na+/-/K+/-ATPase (delta V = -3.5 +/- 1.0 mV, n = 4, P = 0.68). When pericytes were grown for 3 days in culture medium with elevated glucose concentrations (22.5 mmol/l), the resting membrane voltage and the insulin-induced hyperpolarization were not significantly altered. CONCLUSION: Insulin hyperpolarizes the membrane voltage of retinal pericytes probably mediated by activation of apamin-sensitive Ca(2+)-activated potassium channels. Therefore, hormonal modulation of membrane voltage by insulin might be an important factor in the regulation of pericyte contractility and retinal microcirculation under physiological conditions and in diabetes mellitus.

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