Vasopressin induces arachidonic acid release through pertussis toxin-sensitive GTP-binding protein in aortic smooth muscle cells: Independence from phosphoinositide hydrolysis

1993 ◽  
Vol 53 (2) ◽  
pp. 169-175 ◽  
Author(s):  
Yoshiaki Ito ◽  
Osamu Kozawa ◽  
Haruhiko Tokuda ◽  
Jun Kotoyori ◽  
Yutaka Oiso
Keyword(s):  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Pertussis Toxin ◽  
Muscle Cells ◽  
Arachidonic Acid Release ◽  
Gtp Binding Protein ◽  
Aortic Smooth Muscle ◽  
Gtp Binding ◽  
Acid Release

Vasopressin activates phospholipase D through pertussis toxin-insensitive GTP-binding protein in aortic smooth muscle cells: function of Ca2+/calmodulin

1995 ◽  
Vol 73 (3-4) ◽  
pp. 191-199 ◽  
Author(s):  
Masaichi Miwa ◽  
Atsushi Suzuki ◽  
Yasuko Watanabe ◽  
Junji Shinoda ◽  
Yutaka Oiso ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Phospholipase D ◽  
Pertussis Toxin ◽  
Binding Protein ◽  
Muscle Cells ◽  
Gtp Binding Protein ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Gtp Binding

In the present study, we examined the effect of vasopressin (AVP) on phosphatidylcholine-hydrolyzing phospholipase D activity in primary cultured rat aortic smooth muscle cells. AVP stimulation of choline formation was dose dependent. The time-course was quite different from those of inositol phosphates. The effect of AVP on the formation of inositol phosphates (EC50 was 3 nM) was more potent than that on the formation of choline (EC50 was 30 nM). 12-O-Tetradecanoylphorbol-13-acetate (TPA), an activator of protein kinase C (PKC), stimulated the formation of choline. However, 4α-phorbol 12,13-didecanoate, which is inactive for PKC, had little effect. Staurosporine, an inhibitor of protein kinases, which inhibited the TPA-induced formation of choline, had little effect on the AVP-induced formation of choline. Neither calphostin C, a highly specific PKC inhibitor, nor PKC down-regulation with TPA affected AVP-induced formation of choline. A combination of AVP and TPA additively stimulated the formation of choline. The depletion of extracellular Ca2+ by (ethylenebis(oxyethylenenitrilo))tetraacetic acid significantly reduced the AVP-induced formation of choline. W-7, an antagonist of calmodulin, inhibited the AVP-induced formation of choline in a dose-dependent manner. NaF, an activator for GTP-binding protein (G-protein), stimulated the formation of choline. However, the formation of choline by a combination of AVP and NaF was not additive. Pertussis toxin had little effect on the AVP-induced formation of choline. These results strongly suggest that AVP stimulates phospholipase D in a Ca2+/calmodulin-dependent manner in aortic smooth muscle cells, that a pertussis-toxin-insensitive G-protein is involved in the AVP-induced phospholipase D activation, and furthermore, that PKC is not essential for the activation.Key words: vasopressin, phospholipase D, protein kinase C, calmodulin, GTP-binding protein, aortic smooth muscle cells.

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