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Endothelial cell shrinkage increases permeability through a Ca²⁺-dependent pathway in single frog mesenteric microvessels

M. Kajimura and F. E. Curry

We tested whether calcium (Ca²⁺)-dependent mechanisms were essential for our previous observation that a change in the endothelial cell (EC)-extracellular matrix (ECM) attachment caused an increase in microvessel hydraulic permeability (L_p) after exposure to hypertonic solutions in single perfused mesenteric microvessels in pithed frogs (Rana pipiens).

In microvessels where integrin-dependent EC-ECM attachments were disrupted by pretreatment with the peptide Gly-Arg-Gly-Asp-Thr-Pro (GRGDTP; 0·3 mmol l^-1), we measured microvessel L_p after exposure to hypertonic solutions under experimental conditions that reduced Ca²⁺ influx into endothelial cells.

High K⁺ solutions (59·7 and 100 mmol l^-1 K⁺) were used to depolarize the endothelial membrane and therefore to reduce the electrochemical driving force for Ca²⁺ influx through conductive Ca²⁺ channels. These solutions abolished the increase in L_p caused by hypertonic solutions in the microvessels pretreated with GRGDTP.

We previously suggested that the removal of albumin from the perfusate may reduce EC-ECM attachment because hypertonic solutions increased the L_p of microvessels above that due to removal of albumin alone. This additional increase in L_p was attenuated by the 59·7 mmol l^-1 K⁺ solution and was completely abolished by the 100 mmol l^-1 K⁺ solution.

Bumetanide, an inhibitor of the Na⁺-K⁺-2Cl^- co-transporter and one of the mechanisms of regulatory volume increase after exposure to hypertonic solutions in endothelial cells, did not change the response of microvessels to high K⁺ solutions.

Our findings indicate that Ca²⁺ entry into endothelial cells via passive conductance channels is necessary to increase microvessel L_p after exposure to hypertonic solutions in microvessels where EC-ECM attachments are disrupted.

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