Ca2+ entry through conductive pathway modulates receptor-mediated increase in microvessel permeability

Ping He, X. Zhang, F. E. Curry

Research output: Contribution to journalArticle

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Abstract

We investigated the rela-tionship between receptor-mediated increases in cytoplasmic Ca2+ concentration ([Ca2+]i) and increased microvessel permeability. In individually perfused venular microvessels of frog mesentery exposed to 10 μM ATP, [Ca2+]i increased from 59 ± 7 to 172 ± 21 nM within l min and then fell back toward control values. The corresponding peak increase in the hydraulic conductivity (Lp) of the microvessel wall was 5.7 ± 0.5-fold relative to control. After removal of extracellular Ca2+, there was no significant increase in Lp, and the initial increase in [Ca2+]i was attenuated but not abolished. Depolarization of the endothelial cell membrane with high-K+ Ringer solution reduced the peak increase in [Ca2+]i to 106 ± 7 nM and attenuated the increase in Lp 1.8 ± 0.4-fold. The results conform to the hypothesis that Ca2+ entry into endothelial cells is required for acute increase in venular microvessel permeability by inflammatory agents and that the pathway for Ca2+ entry has the properties of a passive conductance pathway. Similar conclusions were reached in previous experiments in frog microvessels exposed to Ca2+ ionophores and perfusates with no plasma proteins. In venular microvessels of hamster mesentery exposed to ATP and bradykinin, a similar pathway for Ca2+ entry was demonstrated in the present experiments. We did not measure permeability changes in hamster microvessels in this study, but these microvessels respond to histamine arid ionophores with a transient increase in permeability to macromolecules similar to that measured in frog microvessels [Am. J. Physiol. 268 (Heart Circ. Physiol. 37): H1982-H1991, 1995].

Original languageEnglish (US)
JournalAmerican Journal of Physiology
Volume271
Issue number6 PART 2
StatePublished - Dec 1 1996

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Microvessels
Permeability
Anura
Mesentery
Ionophores
Cricetinae
Endothelial Cells
Adenosine Triphosphate
Bradykinin
Histamine
Blood Proteins
Cell Membrane

All Science Journal Classification (ASJC) codes

  • Physiology (medical)

Cite this

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abstract = "We investigated the rela-tionship between receptor-mediated increases in cytoplasmic Ca2+ concentration ([Ca2+]i) and increased microvessel permeability. In individually perfused venular microvessels of frog mesentery exposed to 10 μM ATP, [Ca2+]i increased from 59 ± 7 to 172 ± 21 nM within l min and then fell back toward control values. The corresponding peak increase in the hydraulic conductivity (Lp) of the microvessel wall was 5.7 ± 0.5-fold relative to control. After removal of extracellular Ca2+, there was no significant increase in Lp, and the initial increase in [Ca2+]i was attenuated but not abolished. Depolarization of the endothelial cell membrane with high-K+ Ringer solution reduced the peak increase in [Ca2+]i to 106 ± 7 nM and attenuated the increase in Lp 1.8 ± 0.4-fold. The results conform to the hypothesis that Ca2+ entry into endothelial cells is required for acute increase in venular microvessel permeability by inflammatory agents and that the pathway for Ca2+ entry has the properties of a passive conductance pathway. Similar conclusions were reached in previous experiments in frog microvessels exposed to Ca2+ ionophores and perfusates with no plasma proteins. In venular microvessels of hamster mesentery exposed to ATP and bradykinin, a similar pathway for Ca2+ entry was demonstrated in the present experiments. We did not measure permeability changes in hamster microvessels in this study, but these microvessels respond to histamine arid ionophores with a transient increase in permeability to macromolecules similar to that measured in frog microvessels [Am. J. Physiol. 268 (Heart Circ. Physiol. 37): H1982-H1991, 1995].",
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Ca2+ entry through conductive pathway modulates receptor-mediated increase in microvessel permeability. / He, Ping; Zhang, X.; Curry, F. E.

In: American Journal of Physiology, Vol. 271, No. 6 PART 2, 01.12.1996.

Research output: Contribution to journalArticle

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