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Endothelin receptors and their cellular signal transduction mechanism in human cultured prostatic smooth muscle cells
Author(s) -
Saita Yuji,
Koizumi Tomonobu,
Yazawa Hidenori,
Morita Takashi,
Takenaka Toichi,
Honda Kazuo
Publication year - 1997
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0701179
Subject(s) - pertussis toxin , receptor , endothelin receptor , signal transduction , microbiology and biotechnology , biology , mechanism of action , endothelin 1 , g protein , endocrinology , medicine , in vitro , biochemistry
Endothelin (ET) receptors, and their cellular signal transduction mechanism, were characterized in a primary culture of human prostatic smooth muscle cells (HP cell). [ 125 I]‐ET‐1 and [ 125 I]‐ET‐3 binding studies revealed that both ET A and ET B receptors were present in the HP cells, and the ratio of ET A to ET B receptors was 1.4:1. Analysis of ET receptor mRNA by reverse transcription‐polymerase chain reaction also demonstrated that HP cells express both ET A and ET B receptors. ET‐1 and ET‐3 increased intracellular free Ca 2+ concentration ([Ca 2+ ] i ) in the HP cells in a concentration‐dependent manner. Use of subtype selective antagonists BQ‐123 and BQ‐788, indicated that both ET A and ET B receptors were coupled to an increase in [Ca 2+ ] i . Pretreatment of the cells with pertussis toxin resulted in a significant but partial attenuation of the [Ca 2+ ] i increase mediated through the ET A and ET B receptors. However, sensitivity to pertussis toxin (PTX) was significantly different between them. In conclusion, HP cells possess ET A and ET B receptors. Further, these two endothelin receptor subtypes evoke an increase in [Ca 2+ ] i possibly via the action of different GTP‐binding proteins.British Journal of Pharmacology (1997) 121 , 687–694; doi: 10.1038/sj.bjp.0701179