We investigated the hypothesis that an increase in cytoplasmic calcium ion concentration, [Ca2+](i), is one of the mechanisms responsible for increased microvessel permeability. We loaded the cells forming the walls of individually perfused microvessels in frog mesentery with fura-2 and measured [Ca2+](i) in the control state and after adding the Ca2+ ionophore ionomycin to the perfusate. [Ca2+](i) in the control state was 65±6 nM and increased to an initial peak of 285±29 nM after 1-3 min. After 4, 6, and 10 min, [Ca2+](i) was 199±18, 163±16, and 129±9 nM, respectively. [Ca2+](i) fell back to 77±7 nM after ionophore was removed. In similar experiments, hydraulic conductivity (L(p)) increased to a peak of 9.5 times control after 1-3 min, then fell to 2.0 times control after 6 min. L(p) remained elevated at this level for as long as ionophore was present in the perfusate. [Ca2+](i) modulates the initial and sustained phases of the permeability increase. Both processes depend on external Ca2+ influx. Our experiments provide the first direct measurement of [Ca2+](i) during a change in the permeability of an intact microvessel.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||5 27-5|
|State||Published - 1990|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Physiology (medical)