Objective. To investigate the effects of several vasoactive peptides on the development of arterial restenosis after balloon angioplasty.Methods. In rat aortic artery restenosis model produced by denudation of aortic endothelia

we observed changes of endothelin （ET）

angiotensin II （AII）

calcitonin gene-related peptide （CGRP） and adrenomedullin （Adm） in plasma and aorta with radioimmunoassay and expression of hypertension-related gene （HRG-1） with semi-quantitative RT-PCR

and studied the effects of these peptides on intimal hyperplasia

intima/media ratio and MAPK activities of aortic artery after angioplasty respectively. Furthermore

in cultured cells

we studied the effects of these peptides on vascular smooth muscle cell （VSMC） proliferation and expression of HRG-1 of VSMC from spontaneously hypertensive rats （SHR） and Wistar-Kyoto （WKY） rats with 3H-TdR incorporation and RT-PCR respectively.Results. After angioplasty

the levels of ET and AII in plasma and aorta significantly increased

accompanied with VSMC proliferation and neointima hyperplasia. On day 10 after angioplasty

the levels of ET in plasma and aorta increased by 69% and 124% respectively

compared with sham group （ P <0. 01）; and the level of aortic AII increased by 80% （ P < 0. 01）. Antiserum against ET or inhibitors of angiotensin converting enzyme （ACE） could significantly inhibit the proliferation of VSMC and neointima formation. Compared with the sham group

on day 3 after angioplasty

the CGRP levels in plasma and aorta increased by 64% and 89% respectively （ P < 0. 01） and the Adm levels in plasma and tissue increased by 129% and 102% respectively （ P < 0. 01）. On day 10

intravenous administration of CGRP significantly inhibited the proliferation of VSMC and neointima formation induced by balloon aortic injury（by 66% and 79% respectively

P <0. 01）. In addition

ET and AII attenuated the expression of HRG-1 in aorta and stimulated mitogen-activated protein kinase （MAPK） activity

while CGRP and Adm potentiated the expression of HRG-1 and inhibited MAPK.Conclusions. ET and AII can stimulate the proliferation of injured intima while CGRP and Adm have an an-ti-hyperplasia effect after angioplasty. These 4 peptides are involved in the regulation of VSMC proliferation and affect the development of vascular restenosis by regulating the expression of HRG-1 and MAPK activity.