INVOLVEMENT OF EP(3) SUBTYPE OF PROSTAGLANDIN-E RECEPTORS IN PGE(2)-INDUCED ENHANCEMENT OF THE BRADYKININ RESPONSE OF NOCICEPTORS

被引：48

作者：

KUMAZAWA, T

MIZUMURA, K

KODA, H

机构：

[1] Department of Neural Regulation, Research Institute of Environmental Medicine, Nagoya University, Chikusa-ku, Nagoya, 464-01, Furo-cho

来源：

BRAIN RESEARCH | 1993年 / 632卷 / 1-2期

关键词：

POLYMODAL RECEPTOR; VISCERAL NOCICEPTOR; SENSITIZATION; PROSTAGLANDIN E2; BRADYKININ; EP RECEPTOR SUBTYPE; CAMP; NERVE DISCHARGE;

D O I：

10.1016/0006-8993(93)91169-S

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Prostaglandin E(2) augments bradykinin-induced discharges of polymodal receptors as studied in vitro preparations. The antagonist and agonists for three subtypes of EP receptors were used to determine which subtype is involved in this phenomenon. The agonist for EP(3) (M&B28767) simulated the PGE(2)-induced effect but not for EP(2) (butaprost). The antagonist for EP(1) (AH6809) did not suppress the effect. These findings indicate the involvement of the EP(3) receptor subtype in the effect.

引用

页码：321 / 324

页数：4

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