Pressure is proinflammatory in lung venular capillaries

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Abstract

Endothelial responses may contribute importantly to the pathology of high vascular pressure. In lung venular capillaries, we determined endothelial [Ca2+]i by the fura-2 ratioing method and fusion pore formation by quantifying the fluorescence of FM1-43. Pressure elevation increased endothelial [Ca2+]i. Concomitantly evoked exocytotic events were evident in a novel spatial-temporal pattern of fusion pore formation. Fusion pores formed predominantly at vascular branch points and colocalized with the expression of P-selectin. Blockade of mechanogated Ca2+ channels inhibited these responses, identifying entry of external Ca2+ as the critical triggering mechanism. These endothelial responses point to a proinflammatory effect of high vascular pressure that may be relevant in the pathogenesis of pressure-induced lung disease.

Authors

Wolfgang M. Kuebler, Xiaoyou Ying, Baljit Singh, Andrew C. Issekutz, Jahar Bhattacharya