HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 564/3/817    most recent jphysiol.2005.083220v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Glass, C. A. Articles by Bates, D. O. Search for Related Content PubMed PubMed Citation Articles by Glass, C. A. Articles by Bates, D. O.

¹ Microvascular Research Laboratories, Department of Physiology, Preclinical Veterinary School, Southwell Street, University of Bristol, Bristol BS2 8EJ, UK
² Department of Physiology and Membrane Biology, University of California at Davis, Davis, CA 95616, USA

Vascular permeability is assumed to be regulated by the cytosolic Ca²⁺ concentration ([Ca²⁺]_c) of the endothelial cells. When permeability is increased, however, the maximum [Ca²⁺]_c appears to occur after the maximum permeability increase, suggesting that Ca²⁺-dependent mechanisms other than the absolute Ca²⁺ concentration may regulate permeability. Here we investigate whether the rate of increase of the [Ca²⁺]_c (d[Ca²⁺]_c/dt) may more closely approximate the time course of the permeability increase. Hydraulic conductivity (L_p) and endothelial [Ca²⁺]_c were measured in single perfused frog mesenteric microvessels in vivo. The relationships between the time courses of the increased L_p, [Ca²⁺]_c and d[Ca²⁺]_c/dt were examined. L_p peaked significantly earlier than [Ca²⁺]_c in all drug treatments examined (Ca²⁺ store release, store-mediated Ca²⁺ influx, and store-independent Ca²⁺ influx). When L_p was increased in a store-dependent manner the time taken for L_p to peak (3.6 ± 0.9 min during store release, 1.2 ± 0.3 min during store-mediated Ca²⁺ influx) was significantly less than the time taken for [Ca²⁺]_c to peak (9.2 ± 2.8 min during store release, 2.1 ± 0.7 min during store-mediated influx), but very similar to that for the peak d[Ca²⁺]_c/dt to occur (4.3 ± 2.0 min during store release, 1.1 ± 0.5 min during Ca²⁺ influx). Additionally, when the increase was independent of intracellular Ca²⁺ stores, L_p (0.38 ± 0.03 min) and d[Ca²⁺]_c/dt (0.30 ± 0.1 min) both peaked significantly before the [Ca²⁺]_c (1.05 ± 0.31 min). These data suggest that the regulation of vascular permeability by endothelial cell Ca²⁺ may be regulated by the rate of change of the [Ca²⁺]_c rather than the global [Ca²⁺].

(Received 13 January 2005; accepted after revision 15 February 2005; first published online 17 February 2005)
Corresponding author D. O. Bates: Microvascular Research Laboratories, Department of Physiology, School of Veterinary Sciences, Southwell Street, University of Bristol, Bristol BS2 8EJ, UK. Email: dave.bates{at}bristol.ac.uk

This article has been cited by other articles:

				R. R. Foster, S. C. Slater, J. Seckley, D. Kerjaschki, D. O. Bates, P. W. Mathieson, and S. C. Satchell Vascular Endothelial Growth Factor-C, a Potential Paracrine Regulator of Glomerular Permeability, Increases Glomerular Endothelial Cell Monolayer Integrity and Intracellular Calcium Am. J. Pathol., October 1, 2008; 173(4): 938 - 948. [Abstract] [Full Text] [PDF]

				F.-R. E. Curry and C. A. Glass TRP Channels and the Regulation of Vascular Permeability: New Insights From the Lung Microvasculature Circ. Res., October 27, 2006; 99(9): 915 - 917. [Full Text] [PDF]

				C. A. Glass, S. J. Harper, and D. O. Bates The anti-angiogenic VEGF isoform VEGF165b transiently increases hydraulic conductivity, probably through VEGF receptor 1 in vivo J. Physiol., April 1, 2006; 572(1): 243 - 257. [Abstract] [Full Text] [PDF]