Vasopressin induces arachidonic acid release through pertussis toxin-sensitive GTP-binding protein in aortic smooth muscle cells: Independence from phosphoinositide hydrolysis
✍ Scribed by Yoshiaki Ito; Osamu Kozawa; Haruhiko Tokuda; Jun Kotoyori; Yutaka Oiso
- Publisher
- John Wiley and Sons
- Year
- 1993
- Tongue
- English
- Weight
- 685 KB
- Volume
- 53
- Category
- Article
- ISSN
- 0730-2312
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✦ Synopsis
We previously reported that pertussis toxin (PTX) had little effect on arginine vasopressin-induced formation of inositol trisphosphate (IP3) in rat aortic smooth muscle cells [Kondo et al.: Biochemical and Biophysical Research Communications 161 :677-682, 19891. In the present study, we investigated the mechanism of vasopressininduced arachidonic acid release in rat aortic smooth muscle cells. Vasopressin stimulated both the release of arachidonic acid and the formation of IP3 dose dependently in the range between 10 p M and 1 kM. The effect of vasopressin on arachidonic acid release was more potent than that on the formation of IP3. Quinacrine, a phospholipase A? inhibitor, significantly suppressed the vasopressin-induced arachidonic acid release but had little effect on the formation of inositol phosphates. NaF, a GTP-binding protein activator, mimicked vasopressin by stimulating the arachidonic acid release. The arachidonic acid release stimulated by a combination of vasopressin and NaF was not additive. PTX partially but significantly suppressed the vasopressin-induced arachidonic acid release. In the cell membranes, PTX catalyzed ADP-ribosylation of a protein with an Mr of about 40,000. Pretreatment of membranes with 0.1 pM vasopressin in the presence of 2.5 m M MgC12 and 100 kM GTP markedly attenuated this PTX-catalyzed ADP-ribosylation of the protein in a time-dependent manner. These results strongly suggest that PTX-sensitive GTP-binding protein is involved in the coupling of vasopressin receptor to phospholipase A? in primary cultured rat aortic smooth muscle cells. ' 1993 WiIey-Liss, Inc.