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Nephrology Dialysis Transplantation, Vol 13, Issue 8 2047-2052, Copyright © 1998 by Oxford University Press

ORIGINAL ARTICLES

Bradykinin stimulates the intracellular calcium activity in human mesothelial cells

M Andre, S Rahimi, P Schollmeyer and H Pavenstadt
Department of Medicine, Department of Nephrology, University of Freiburg, Freiburg, Germany; Correspondence to: H Pavenstadt, Medizinische Universitatsklinik, Abt. IV, Labor C4, Hugstetter Strasse 55, D-79106 Freiburg, Germany

Aim. The aim of this study was to investigate the influence of bradykinin on the intracellular calcium activity ([Ca2+]i) in human mesothelial cells in culture. Results. Bradykinin (1-1000 nmol/l) caused a concentration-dependent and reversible increase of [Ca2+]i in mesothelial cells (n = 94); 10 nmol/l bradykinin increased [Ca2+]i from 23 ± 9 to 670 ± 170 nmol/l (n = 36). The pattern of the bradykinin-induced [Ca2+]i increase was biphasic with a transient [Ca2+]i peak, which was followed by a sustained [Ca2+]i plateau. The bradykinin-mediated [Ca2+]i plateau, but not the peak was inhibited in a solution with an extracellular reduced Ca2+ concentration (from 1000 to 1 &mgr;mol/l, n = 11). Flufenamate (⩾10 &mgr;mol/l), an inhibitor of non-selective ion channels abolished the bradykinin-mediated increase of [Ca2+]i, whereas the L-type Ca2+ channel blocker nicardipine (10 &mgr;mol/l) had no effect (n = 3-5). The [Ca2+]i response to bradykinin was inhibited by the BK2 antagonist Hoe 140 (IC50 ± k7 nmol/l, n = 30). Conclusions. The data indicate that bradykinin stimulates [Ca2+]i in mesothelial cells by a release of Ca2+ from intracellular stores and an influx from Ca2+ through non-selective channels via a BK2 receptor. Keywords: bradykinin; mesothelial cells; intracellular calcium activity
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