Depolarization modulates endothelial cell calcium influx and microvessel permeability

P. He, F. E. Curry

Research output: Contribution to journalArticle

57 Citations (Scopus)

Abstract

We investigated the mechanisms whereby high-potassium (57.9 mM) Ringer solutions attenuate the increase in permeability caused when microvessels are exposed to the calcium ionophores ionomycin and A23187 (5 μM). In single perfused microvessels we measured cytoplasmic calcium concentration, [Ca2+](i), in the cells forming the microvessel wall and the hydraulic conductivity, L(p), to follow changes in the permeability of the microvessel walls. In normal Ringer solution, [Ca2+](i) was increased to an initial peak value of 226 ± 12 nM after exposure to calcium ionophores; the corresponding increase in microvessel L(p) was 10.3 ± 2.6 times control. With high-potassium solutions, the peak value of [Ca2+](i) was 133 ± 12nM and L(p) was increased to only 2.5 ± 0.7 times control. Increasing extracellular calcium from 1.1 to 5 mM with high potassium restored the initial peak value of [Ca2+](i) to 303 ± 38 nM. The increases in both [Ca2+](i) and L(p) were abolished in calcium-free solutions. If high-potassium solutions depolarize the cells forming the microvessel wall as indicated by the membrane potential-sensitive dye bisoxonol, then the magnitude of the initial increase in [Ca2+](i) could be accounted for by changes in the electrochemical driving force through conductive channels for calcium ion. Our results conform to the hypothesis that the permeability properties of microvessels are modulated by changes in the membrane potential of the endothelial cells and/or pericytes forming the microvessel wall.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume261
Issue number4 30-4
StatePublished - 1991

Fingerprint

Microvessels
Permeability
Endothelial Cells
Calcium
Potassium
Calcium Ionophores
Membrane Potentials
Pericytes
Ionomycin
Calcimycin
Calcium Channels
Coloring Agents

Keywords

  • A23187
  • calcium ionophores
  • capillary permeability
  • conductive calcium pathways
  • cytoplasmic calcium
  • fura-2 measurement
  • hydraulic conductivity
  • ionomycin
  • membrane potential
  • single perfused microvessels

ASJC Scopus subject areas

  • Physiology

Cite this

Depolarization modulates endothelial cell calcium influx and microvessel permeability. / He, P.; Curry, F. E.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 261, No. 4 30-4, 1991.

Research output: Contribution to journalArticle

@article{377f3ecc9ab24c4d9ae9ecf3068af3da,
title = "Depolarization modulates endothelial cell calcium influx and microvessel permeability",
abstract = "We investigated the mechanisms whereby high-potassium (57.9 mM) Ringer solutions attenuate the increase in permeability caused when microvessels are exposed to the calcium ionophores ionomycin and A23187 (5 μM). In single perfused microvessels we measured cytoplasmic calcium concentration, [Ca2+](i), in the cells forming the microvessel wall and the hydraulic conductivity, L(p), to follow changes in the permeability of the microvessel walls. In normal Ringer solution, [Ca2+](i) was increased to an initial peak value of 226 ± 12 nM after exposure to calcium ionophores; the corresponding increase in microvessel L(p) was 10.3 ± 2.6 times control. With high-potassium solutions, the peak value of [Ca2+](i) was 133 ± 12nM and L(p) was increased to only 2.5 ± 0.7 times control. Increasing extracellular calcium from 1.1 to 5 mM with high potassium restored the initial peak value of [Ca2+](i) to 303 ± 38 nM. The increases in both [Ca2+](i) and L(p) were abolished in calcium-free solutions. If high-potassium solutions depolarize the cells forming the microvessel wall as indicated by the membrane potential-sensitive dye bisoxonol, then the magnitude of the initial increase in [Ca2+](i) could be accounted for by changes in the electrochemical driving force through conductive channels for calcium ion. Our results conform to the hypothesis that the permeability properties of microvessels are modulated by changes in the membrane potential of the endothelial cells and/or pericytes forming the microvessel wall.",
keywords = "A23187, calcium ionophores, capillary permeability, conductive calcium pathways, cytoplasmic calcium, fura-2 measurement, hydraulic conductivity, ionomycin, membrane potential, single perfused microvessels",
author = "P. He and Curry, {F. E.}",
year = "1991",
language = "English (US)",
volume = "261",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "4 30-4",

}

TY - JOUR

T1 - Depolarization modulates endothelial cell calcium influx and microvessel permeability

AU - He, P.

AU - Curry, F. E.

PY - 1991

Y1 - 1991

N2 - We investigated the mechanisms whereby high-potassium (57.9 mM) Ringer solutions attenuate the increase in permeability caused when microvessels are exposed to the calcium ionophores ionomycin and A23187 (5 μM). In single perfused microvessels we measured cytoplasmic calcium concentration, [Ca2+](i), in the cells forming the microvessel wall and the hydraulic conductivity, L(p), to follow changes in the permeability of the microvessel walls. In normal Ringer solution, [Ca2+](i) was increased to an initial peak value of 226 ± 12 nM after exposure to calcium ionophores; the corresponding increase in microvessel L(p) was 10.3 ± 2.6 times control. With high-potassium solutions, the peak value of [Ca2+](i) was 133 ± 12nM and L(p) was increased to only 2.5 ± 0.7 times control. Increasing extracellular calcium from 1.1 to 5 mM with high potassium restored the initial peak value of [Ca2+](i) to 303 ± 38 nM. The increases in both [Ca2+](i) and L(p) were abolished in calcium-free solutions. If high-potassium solutions depolarize the cells forming the microvessel wall as indicated by the membrane potential-sensitive dye bisoxonol, then the magnitude of the initial increase in [Ca2+](i) could be accounted for by changes in the electrochemical driving force through conductive channels for calcium ion. Our results conform to the hypothesis that the permeability properties of microvessels are modulated by changes in the membrane potential of the endothelial cells and/or pericytes forming the microvessel wall.

AB - We investigated the mechanisms whereby high-potassium (57.9 mM) Ringer solutions attenuate the increase in permeability caused when microvessels are exposed to the calcium ionophores ionomycin and A23187 (5 μM). In single perfused microvessels we measured cytoplasmic calcium concentration, [Ca2+](i), in the cells forming the microvessel wall and the hydraulic conductivity, L(p), to follow changes in the permeability of the microvessel walls. In normal Ringer solution, [Ca2+](i) was increased to an initial peak value of 226 ± 12 nM after exposure to calcium ionophores; the corresponding increase in microvessel L(p) was 10.3 ± 2.6 times control. With high-potassium solutions, the peak value of [Ca2+](i) was 133 ± 12nM and L(p) was increased to only 2.5 ± 0.7 times control. Increasing extracellular calcium from 1.1 to 5 mM with high potassium restored the initial peak value of [Ca2+](i) to 303 ± 38 nM. The increases in both [Ca2+](i) and L(p) were abolished in calcium-free solutions. If high-potassium solutions depolarize the cells forming the microvessel wall as indicated by the membrane potential-sensitive dye bisoxonol, then the magnitude of the initial increase in [Ca2+](i) could be accounted for by changes in the electrochemical driving force through conductive channels for calcium ion. Our results conform to the hypothesis that the permeability properties of microvessels are modulated by changes in the membrane potential of the endothelial cells and/or pericytes forming the microvessel wall.

KW - A23187

KW - calcium ionophores

KW - capillary permeability

KW - conductive calcium pathways

KW - cytoplasmic calcium

KW - fura-2 measurement

KW - hydraulic conductivity

KW - ionomycin

KW - membrane potential

KW - single perfused microvessels

UR - http://www.scopus.com/inward/record.url?scp=0025942193&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025942193&partnerID=8YFLogxK

M3 - Article

C2 - 1928406

AN - SCOPUS:0025942193

VL - 261

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

SN - 1931-857X

IS - 4 30-4

ER -