June 1992
Volume 33, Issue 7
Free
Articles  |   June 1992
Membrane potentials in retinal capillary pericytes: excitability and effect of vasoactive substances.
Author Affiliations
  • H Helbig
    Department of Ophthalmology, Universitätsklinikum Steglitz, Freie Universität Berlin, FRG.
  • S Kornacker
    Department of Ophthalmology, Universitätsklinikum Steglitz, Freie Universität Berlin, FRG.
  • S Berweck
    Department of Ophthalmology, Universitätsklinikum Steglitz, Freie Universität Berlin, FRG.
  • F Stahl
    Department of Ophthalmology, Universitätsklinikum Steglitz, Freie Universität Berlin, FRG.
  • A Lepple-Wienhues
    Department of Ophthalmology, Universitätsklinikum Steglitz, Freie Universität Berlin, FRG.
  • M Wiederholt
    Department of Ophthalmology, Universitätsklinikum Steglitz, Freie Universität Berlin, FRG.
Investigative Ophthalmology & Visual Science June 1992, Vol.33, 2105-2112. doi:
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      H Helbig, S Kornacker, S Berweck, F Stahl, A Lepple-Wienhues, M Wiederholt; Membrane potentials in retinal capillary pericytes: excitability and effect of vasoactive substances.. Invest. Ophthalmol. Vis. Sci. 1992;33(7):2105-2112.

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Abstract

Retinal capillary pericytes are believed to have a contractile function and to regulate retinal blood flow at the microvascular level. Membrane potential is an important control element for contractility in smooth muscle cells. In the present study, bovine retinal capillary pericytes have been grown in tissue culture and membrane potentials have been measured using glass microelectrodes. Resting potentials averaged -31 +/- 7 mV (n = 203). Relative K+ conductance was low, with a transference number for K+ of 0.16. Readdition of K+ to K(+)-depleted cells transiently hyperpolarized the membrane potential, probably by stimulating the electrogenic Na+/K+ transport. Repetitive spike-like depolarizations (action potentials) were induced by stimulating the Na+/K(+)-ATPase, by applying norepinephrine (10(-5) mol/l), and by adding 10 mmol/l Ba2+. These action potentials depended on the presence of extracellular Ca2+ and were inhibited by the Ca2+ antagonist nifedipine (10(-6) mol/l). Norepinephrine (10(-5) mol/l) depolarized the membrane by 7.4 +/- 3.5 mV (mean +/- SD, n = 49). This response was blocked by the alpha 1-antagonist prazosin (10(-5) mol/l). Histamine also led to a membrane depolarization of 8.6 +/- 2.8 mV (n = 49), which could be inhibited by the H1-antagonist diphenhydramine. Endothelin (10(-7) mol/l), vasopressin (10(-6) mol/l), and acetylcholine (10(-4) mol/l) had no major effects on membrane potential. The conclusion is that retinal capillary pericytes are excitable cells and react to several vasoactive substances.

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