-transparent.png){kind=logo}
We examined the effects of alterations in endothelial cell volume on transendothelial albumin permeability. Studies were done using a confluent monolayer of bovine pulmonary artery endothelial cells grown on gelatinized microporous filters. When endothelial cells were exposed to media made hypertonic with 200 mM mannitol, the intracellular volume (measured with 14C-urea) decreased twofold and remained decreased over a 30-minute time-span, thus showing no significant regulatory volume increase (RVI) within this time period. When endothelial cells were exposed to hypotonic media, intracellular volume rapidly doubled within 2 minutes, and then decreased to baseline values within 10 minutes in spite of the sustained hypotonic environment, a process known as regulatory volume decrease (RVD). We also measured the transendothelial flux of 125I-albumin with the cells exposed to the same osmotic changes. We observed that only under hypertonic conditions was there a significant change in the 125I-albumin permeability. These results indicate that the pulmonary artery endothelial cells in culture alter their cell volume when exposed to variations in the osmotic environment, and also show RVD in response to hypotonic conditions but no RVI within 40 minutes after exposure to hypertonic conditions. The transendothelial albumin permeability did not change under hypotonic conditions but increased under hypertonic conditions. Thus, endothelial cells shrinkage may be an important mechanism of increased endothelial macromolecule permeability. These volume changes may occur in endothelial cells in situ and have a role in inducing alterations in the transendothelial permeability to proteins.
J M Shepard, and
S K Goderie, and
N Brzyski, and
P J Del Vecchio, and
A B Malik, and
H K Kimelberg
July 1991,
Microvascular research,
J M Shepard, and
S K Goderie, and
N Brzyski, and
P J Del Vecchio, and
A B Malik, and
H K Kimelberg
November 2017,
Free radical biology & medicine,
J M Shepard, and
S K Goderie, and
N Brzyski, and
P J Del Vecchio, and
A B Malik, and
H K Kimelberg
November 1986,
Journal of cellular physiology,
J M Shepard, and
S K Goderie, and
N Brzyski, and
P J Del Vecchio, and
A B Malik, and
H K Kimelberg
January 1993,
Agents and actions,
J M Shepard, and
S K Goderie, and
N Brzyski, and
P J Del Vecchio, and
A B Malik, and
H K Kimelberg
March 1993,
The American journal of physiology,
J M Shepard, and
S K Goderie, and
N Brzyski, and
P J Del Vecchio, and
A B Malik, and
H K Kimelberg
February 2006,
Atherosclerosis,
J M Shepard, and
S K Goderie, and
N Brzyski, and
P J Del Vecchio, and
A B Malik, and
H K Kimelberg
January 1986,
Journal of applied physiology (Bethesda, Md. : 1985),
J M Shepard, and
S K Goderie, and
N Brzyski, and
P J Del Vecchio, and
A B Malik, and
H K Kimelberg
May 1989,
Microvascular research,
J M Shepard, and
S K Goderie, and
N Brzyski, and
P J Del Vecchio, and
A B Malik, and
H K Kimelberg
November 1960,
Clinical science,
J M Shepard, and
S K Goderie, and
N Brzyski, and
P J Del Vecchio, and
A B Malik, and
H K Kimelberg
January 1986,
Annals of the New York Academy of Sciences,
