This Article Full Text Full Text (PDF) All Versions of this Article: 43/1/131    most recent 01.HYP.0000105300.74809.4Fv1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dina, J. P. Articles by Paiva, T. B. Search for Related Content PubMed PubMed Citation Articles by Dina, J. P. Articles by Paiva, T. B. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information High Blood Pressure Hazardous Substances DB NITRIC OXIDE Related Collections Restenosis Animal models of human disease Hypertension - basic studies Smooth muscle proliferation and differentiation

(Hypertension. 2004;43:131.)
© 2004 American Heart Association, Inc.

Scientific Contributions

Role of Membrane Potential and Expression of Endothelial Factors in Restenosis After Angioplasty in SHR

From the Department of Biophysics, Escola Paulista de Medicina, Federal University of São Paulo, São Paulo, Brazil.

Correspondence to Therezinha B. Paiva, MD, PhD, Department of Biophysics, Federal University of São Paulo, Rua Botucatu, 862, 04023-032 São Paulo, SP, Brazil. E-mail tbpaiva{at}biofis.epm.br

We examined the roles played by impaired K⁺ channels, diminished nitric oxide (NO) production, endothelin release, and smooth muscle membrane potential in the increased restenosis observed in spontaneously hypertensive rat (SHR) carotid arteries after angioplasty. The SHR carotid was found to be less polarized than that of normotensive Wistar rats (NWR), and it was further depolarized by the ₂ agonist UK 14,304. This response was blocked by iberiotoxin, indicating that calcium-dependent K⁺ channels operate normally in the SHR carotid. Acetylcholine caused a hyperpolarization that was significantly smaller in SHR than in NWR carotids, indicating a deficient release of NO in the SHR. After angioplasty, SHR and NWR vessels were depolarized, returning to baseline after 10 days. In the SHR but not in the NWR the contralateral carotid was also depolarized, and this was prevented by the endothelin A/B receptor antagonist bosentan. After angioplasty, endothelin-1 plasma levels increased in both SHR and NWR, but the increase was significantly more prolonged in SHR. We found that the more pronounced restenosis observed in the SHR carotid after angioplasty is not due to impairment of calcium-dependent K⁺ channels but is related to the relatively depolarized vascular smooth muscles, involving endothelin release caused by reduced NO levels in that strain.

Key Words: rats, spontaneously hypertensive • angioplasty • carotid arteries • muscle smooth, vascular • membranes • endothelin

This article has been cited by other articles:

				S. G. Denniss and J. W. E. Rush Impaired hemodynamics and endothelial vasomotor function via endoperoxide-mediated vasoconstriction in the carotid artery of spontaneously hypertensive rats Am J Physiol Heart Circ Physiol, April 1, 2009; 296(4): H1038 - H1047. [Abstract] [Full Text] [PDF]

				W. J. Gomes and E. Buffolo Coronary stenting and inflammation: implications for further surgical and medical treatment. Ann. Thorac. Surg., May 1, 2006; 81(5): 1918 - 1925. [Abstract] [Full Text] [PDF]