Stimulation of platelet-derived growth factor-induced DNA synthesis by angiotensin II in rabbit vascular smooth muscle cells

1990 ◽  
Vol 168 (1) ◽  
pp. 350-357 ◽  
Author(s):  
Shun-ichi Araki ◽  
Yasuhiro Kawahara ◽  
Ken-ichi Kariya ◽  
Michitoshi Sunako ◽  
Terutaka Tsuda ◽  
...  
1984 ◽  
Vol 247 (5) ◽  
pp. C501-C505 ◽  
Author(s):  
N. E. Owen

Platelet-derived growth factor (PDGF) is known to be a potent mitogenic agent for vascular smooth muscle cells. The effect of PDGF on amiloride-sensitive Na+ influx was investigated in A-10 vascular smooth muscle cells. At a dose which maximally stimulates DNA synthesis, PDGF stimulates net Na+ influx in vascular smooth muscle cells. The PDGF-stimulated Na+ influx is linear over a 5-min time course. PDGF stimulates Na+ influx in a concentration-dependent manner, with a concentration of 0.5 U/ml causing half-maximal inhibition. The effects of PDGF on Na+ influx can be mimicked by 10% fetal bovine serum or by the divalent cation ionophore A23187 (5 microM). Net Na+ influx in response to each of these agents was inhibited by amiloride and by benzamil. PDGF-stimulated net Na+ influx was blocked by the intracellular Ca2+ antagonist 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate as well as by the calmodulin antagonists trifluoperazine, chlorpromazine, and imipramine. These data suggest that PDGF may stimulate an amiloride-sensitive Na+ influx pathway via an elevation in intracellular Ca2+ and formation of a Ca-calmodulin complex. This Na+ influx pathway may be a trigger for PDGF-stimulated DNA synthesis.


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