Abstract
OBJECTIVE: To investigate the mechanisms responsible for variation in the macromolecular leakage (formation of localized leaky sites) in venular microvessels with increased permeability, we examined the hypothesis that cytoplasmic calcium concentration [Ca2+]i, does not increase uniformly within microvessel endothelial cells. METHODS: We loaded the endothelial cells forming the walls of venular microvessels in frog mesentery with fura-2, and imaged [Ca2+]i using a cooled CCD camera. RESULTS: Control [Ca2+]i was close to 60 nM in all regions. Control permeability was uniformly low in all microvessels. Exposure to ionomycin (5 mM) increased [Ca2+]i in a biphasic manner, but not uniformly. There was variation in both time to peak (bimodal distribution) and peak [Ca2+]i (274 +/- 13 nM; mean variation above or below the peak value was 110 nM). Raising extracellular calcium from 1.1 to 5 mM increased the mean variation of [Ca2+]i about peak values. Extravascular leakage of fluorescently labeled albumin or low-density lipoproteins was most prominent at sites where increase in [Ca2+]i were largest. CONCLUSIONS: These data indicate that variation in [Ca2+]i within individual endothelial cells or groups of cells could account, at least in part, for the distribution of localized leakage sites for macromolecules in venular microvessels in the high-permeability state.
Original language | English (US) |
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Pages (from-to) | 213-230 |
Number of pages | 18 |
Journal | Microcirculation (New York, N.Y. : 1994) |
Volume | 1 |
Issue number | 4 |
State | Published - Dec 1994 |
ASJC Scopus subject areas
- Physiology
- Genetics
- Cardiology and Cardiovascular Medicine