Abstract
We investigated the relationship 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 1 min and then fell back toward control values. The corresponding peak increase in the hydraulic conductivity (L(p)) of the microvessel wall was 5.7 ± 0.5-fold relative to control. After removal of extracellular Ca2+, there was no significant increase in L(p), 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 L(p), 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 and 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 language | English (US) |
|---|---|
| Journal | American Journal of Physiology - Heart and Circulatory Physiology |
| Volume | 271 |
| Issue number | 6 40-6 |
| State | Published - 1996 |
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Keywords
- 4-[2-[6-(dioctylamino)-2-naphthalenyl]ethenyl]- 1-(3-sulfopropyl)-pyridinium
- ATP
- bradykinin
- cytoplasmic calcium concentration
- endothelial
- hydraulic conductivity
- individually perfused microvessels
- membrane depolarization
- membrane potential
ASJC Scopus subject areas
- Physiology
- Physiology (medical)
Cite this
Ca2+ entry through conductive pathway modulates receptor-mediated increase in microvessel permeability. / He, P.; Zhang, X.; Curry, F. E.
In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 271, No. 6 40-6, 1996.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Ca2+ entry through conductive pathway modulates receptor-mediated increase in microvessel permeability
AU - He, P.
AU - Zhang, X.
AU - Curry, F. E.
PY - 1996
Y1 - 1996
N2 - We investigated the relationship 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 1 min and then fell back toward control values. The corresponding peak increase in the hydraulic conductivity (L(p)) of the microvessel wall was 5.7 ± 0.5-fold relative to control. After removal of extracellular Ca2+, there was no significant increase in L(p), 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 L(p), 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 and 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].
AB - We investigated the relationship 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 1 min and then fell back toward control values. The corresponding peak increase in the hydraulic conductivity (L(p)) of the microvessel wall was 5.7 ± 0.5-fold relative to control. After removal of extracellular Ca2+, there was no significant increase in L(p), 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 L(p), 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 and 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].
KW - 4-[2-[6-(dioctylamino)-2-naphthalenyl]ethenyl]- 1-(3-sulfopropyl)-pyridinium
KW - ATP
KW - bradykinin
KW - cytoplasmic calcium concentration
KW - endothelial
KW - hydraulic conductivity
KW - individually perfused microvessels
KW - membrane depolarization
KW - membrane potential
UR - http://www.scopus.com/inward/record.url?scp=0030330609&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030330609&partnerID=8YFLogxK
M3 - Article
C2 - 8997296
AN - SCOPUS:0030330609
VL - 271
JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
SN - 1931-857X
IS - 6 40-6
ER -