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Angiotensin II Inhibits Cell Proliferation and Stimulates Protein Synthesis in Rat Glomerulosa Cells

Angiotensin II (Ang Il) is one of the most important stimuli of rat adrenaI glomerulosa cells. The aim of the present study was to investigate whether Ang Il can stimulate cell proliferation and/or hypertrophy and to investigate pathways of these two specific growth responses. Results reveal that a 3-day treatment with Ang Il abolished cell proliferation observed in control cells, but increased protein synthesis. Preincubation with PD98059 (a MEK inhibitor) diminished basal proliferation and affected basal protein synthesis. In contrast, the p38 MAPK inhibitor, SB203580, reversed the inhibitory effect on cell proliferation and abolished the increase in protein synthesis, although the JNK inhibitor had no effect. Time-course studies indeed indicate that Ang II stimulates phosphorylation of p42/p44 mapk (peak at 5 min with a sustained plateau) and of p38 mapk (rapid and transient effect at 2 min), but did not activate JNK. Preincubation with cytochalasin B abolished basal proliferation. Immunofluorescence studies indicate that Ang II favored the formation of a peripheral cortical actin ring, but a depolymerization of the cross-linked F-actin network. Together, these results indicate that a well-developed network of microfilaments is necessary to promote basal cell proliferation, while microfilament disruption are involved in Ang II