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Activation of bradykinin B2 receptors increases calcium entry and intracellular mobilization in C9 liver cells
Author(s) -
GarcíaSáinz J. Adolfo,
AvendañoVázquez S. Eréndira
Publication year - 1999
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216549900202043
Subject(s) - bradykinin , thapsigargin , calcium in biology , bradykinin receptor , intracellular , kallidin , endocrinology , medicine , homologous desensitization , calcium , chemistry , receptor , agonist , icatibant , biology , kinin , biochemistry
10.1080/15216549900202043.abs In C9 rat liver cells bradykinin and kallidin increased (∼ 2‐fold) the intracellular concentration of calcium, but the B1 agonist, des‐Arg9‐bradykinin did not. The effect of bradykinin was inhibited by the B2 antagonists, Hoe 140 and N‐α‐adamantaneacetyl‐D‐Arg‐[Hyp3, Thi5.8, D‐Phe7]‐bradykinin, but not by the B1 antagonist, des‐Arg9‐[Leu8]‐bradykinin. The action of bradykinin was diminished, but not abolished, in medium without calcium. The peptide was able to increase intracellular calcium concentration in cells treated with thapsigargin. Bradykinin action was not observed in cells previously stimulated with this local mediator; however, under the same conditions, angiotensin II induced a clear increase in intracellular calcium concentration. Our data indicate that activation of bradykinin B2 receptors increase intracetllular calcium concentrations by inducing both gating of the cation and intracellular mobilization in C9 liver cells. In addition, homologous desensitization was observed.