大鼠脑中缓激肽/血管紧张素II受体-受体相互作用的放射自显影证据。

Autoradiographic evidence for a bradykinin/angiotensin II receptor-receptor interaction in the rat brain.

作者信息

Fior D R, Hedlund P B, Fuxe K

机构信息

Department of Histology and Neurobiology, Karolinska Institutet, Stockholm, Sweden.

出版信息

Neurosci Lett. 1993 Nov 26;163(1):58-62. doi: 10.1016/0304-3940(93)90228-d.

DOI:10.1016/0304-3940(93)90228-d

PMID:8295734

Abstract

Using angiotensin II (ANG II) to compete with (3-[125I]iodotyrosyl-4, Sar1, Ile8)ANG-II ([125I]Sar1, Ile8)ANG II) for its binding sites in the nucleus of the solitary tract (nTS) and the paraventricular hypothalamic nucleus (PV) bradykinin (10 nM) reduced the IC50 value (48 nM) of ANG II, an action blocked by the bradykinin B2 antagonist HOE-140 (100 nM). In contrast, when analysing the high-affinity site (Kd 3.1 nM) for [125I]ANG II in the nTS bradykinin (10 nM) increased the Kd value. Thus, a central bradykinin/ANG II receptor interaction may exist involving a differential regulation of the high- and low-affinity ANG II receptors in the nTS. This regulation by bradykinin of angiotensin receptors in the nTS may help to explain the central vasopressor effect of bradykinin.

摘要

使用血管紧张素II（ANG II）与（3-[125I]碘酪氨酰-4，Sar1，Ile8）ANG-II（[125I]Sar1，Ile8）ANG II）竞争其在孤束核（nTS）和下丘脑室旁核（PV）中的结合位点，缓激肽（10 nM）降低了ANG II的IC50值（48 nM），缓激肽B2拮抗剂HOE-140（100 nM）可阻断该作用。相反，当分析nTS中[125I]ANG II的高亲和力位点（Kd 3.1 nM）时，缓激肽（10 nM）增加了Kd值。因此，中枢缓激肽/ANG II受体相互作用可能存在，涉及nTS中高亲和力和低亲和力ANG II受体的差异调节。缓激肽对nTS中血管紧张素受体的这种调节可能有助于解释缓激肽的中枢升压作用。