Abnormal proliferative response of the carotid artery of spontaneously hypertensive rats after angioplasty may be related to the depolarized state ofits smooth muscle cells

Citation
Sld. Dalle Lucca et al., Abnormal proliferative response of the carotid artery of spontaneously hypertensive rats after angioplasty may be related to the depolarized state ofits smooth muscle cells, BRAZ J MED, 33(8), 2000, pp. 919-927
Citations number
24
Categorie Soggetti
Medical Research General Topics
Journal title
BRAZILIAN JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH
ISSN journal
0100879X → ACNP
Volume
33
Issue
8
Year of publication
2000
Pages
919 - 927
Database
ISI
SICI code
0100-879X(200008)33:8<919:APROTC>2.0.ZU;2-P
Abstract
Hypertension is one of the major precursors of atherosclerotic vascular dis ease, and vascular smooth muscle abnormal cell replication is a key feature of plaque formation. The present study was conducted to examine the relati onship between hypertension and smooth muscle cell proliferation after ball oon injury and to correlate neointima formation with resting membrane poten tial of uninjured smooth muscle cells, since it has been suggested that alt ered vascular function in hypertension may be related to the resetting of t he resting membrane potential in spontaneously hypertensive rats (SHR). Neo intima formation was induced by balloon injury to the carotid arteries of S HR and renovascular hypertensive rats (1K-1C), as well as in their normoten sive controls, i.e., Wistar Kyoto (WKY) and normal Wistar (NWR) rats. After 14 days the animals were killed and the carotid arteries were submitted to histomorphometric and immunohistochemical analyses. Resting membrane poten tial measurements showed that uninjured carotid arteries from SHR smooth mu scle cells were significantly depolarized (-46.5 +/- 1.9 mV) compared to NW R (-69 +/- 1.4 mV), NWR 1K-1C (-60.8 +/- 1.6 mV), WKY (-67.1 +/- 3.2 mV) an d WKY 1K-1C (-56.9 +/- 1.2 mV). The SHR arteries responded to balloon injur y with an enhanced neointima formation (neo/media = 3.97 +/- 0.86) when com pared to arteries of all the other groups (NWR 0.93 +/- 0.65, NWR 1K-1C 1.2 4 +/- 0.45, WKY 1.22 +/- 0.32, WKY 1K-1C 1.15 +/- 0.74). Our results indica te that the increased fibroproliferative response observed in SHR is not re lated to the hypertensive state but could be associated with the resetting of the carotid smooth muscle cell resting membrane potential to a more depo larized state.