Dh. Wang et al., REGULATION OF PDGF-A - A POSSIBLE MECHANISM FOR ANGIOTENSIN-II-INDUCED VASCULAR GROWTH, American journal of physiology. Heart and circulatory physiology, 38(1), 1995, pp. 356-364
This study was designed to determine the effects of angiotensin II inf
usion on structure of conduit and resistance arteries and to see if th
e effects correlate with changes in platelet-derived growth factor A c
hain (PDGF-A) gene and protein expression. Wistar rats were subcutaneo
usly infused by osmotic minipump with either angiotensin II (ANG II) a
t 200 ng . kg(-1). min(-1) or physiological saline (control) for 14 da
ys. Tail-cuff systolic blood pressure was significantly higher in ANG
II compared with control rats beginning the second day of infusion and
continuing to the end of 2 wk. Both aorta and external spermatic arte
ry (first-order arteriole of the cremaster muscle) developed increased
wall-to-lumen ratios in the ANG II rats, but this occurred by hypertr
ophy of the wall in the aorta and reduction of the lumen in the arteri
ole. Digoxigenin-labeled cRNA probes were used for in situ hybridizati
on of vascular sections to identify PDGF-A mRNA. Gene expression of PD
GF-A in ANG II rats was upregulated in the hypertrophied aorta and the
nonhypertrophied arteriole. With the use of immunocytochemistry techn
iques, PDGF-A and proliferating cell nuclear antigen were increased in
the aorta but not in the arterioles of ANG II rats compared with cont
rol rats. These results suggest that the difference in growth response
between the aorta and the arteriole induced by ANG II may lie in post
transcriptional modification of PDGF-A mRNA, differential control of t
ranslation, or turnover of PDGF-A protein.