Document Detail


Nipradilol inhibits atmospheric pressure-induced cell proliferation in human aortic smooth muscle cells.
MedLine Citation:
PMID:  14726216     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hypertension is a major risk factor for atherosclerosis and the genesis of cardiovascular and cerebrovascular diseases. Therefore, the protection of atherosclerosis progression is one of the purpose of an anti-hypertensive treatment in vascular system. Nitric oxide (NO)-releasing drugs have been reported to have an inhibitory effect on shear stress-induced extracellular signal-regulated kinase (ERK) activation in endothelial cells. For further understanding of the effects of these drugs, the present study focused on the effects on intracellular signal transduction and cell proliferation in cultured human aortic smooth muscle cells (HASMC) under high atmospheric pressure. Three hours of 160-mmHg atmospheric pressure resulted in an approximately 380% increase in cell proliferation compared to non-pressurized controls. Nipradilol (3,4-dihydro-8-(2-hydroxy-3-isopropylaminoproxy)-3-nitroxy-2H-1-benzopyran) (10(-6)M) demonstrated approximately 40% reduction in cell proliferation compared to that shown by pressurized HASMC as a vehicle control. Three hours of 160-mmHg atmospheric pressure resulted in a 25% increase in the amount of activated ERKs. Nipradilol (10(-6)M) demonstrated approximately a 26% reduction in the amount of activated ERKs. NO(x) concentration under the presence of nipradilol (10microM) with HASMC resulted in a 7.2microM of NO production and was 2.4-fold more than that from no dug control (3.0microM). An administration of L-NAME (10(-4)M) supplemented with Nipradilol (10(-6)M) did not show any significant effect on cell proliferation. From these observations, we concluded that nipradilol has an anti-proliferative effect on HASMC under high atmospheric pressure. Nipradilol may act as a nitric oxide inducer from HASMC and suspected to work as a supplement to mitigate the impaired endothelial cell function caused by hypertension.
Authors:
Kenji Iizuka; Noriteru Morita; Takeshi Murakami; Hideaki Kawaguchi
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Pharmacological research : the official journal of the Italian Pharmacological Society     Volume:  49     ISSN:  1043-6618     ISO Abbreviation:  Pharmacol. Res.     Publication Date:  2004 Mar 
Date Detail:
Created Date:  2004-01-16     Completed Date:  2004-09-28     Revised Date:  2009-11-03    
Medline Journal Info:
Nlm Unique ID:  8907422     Medline TA:  Pharmacol Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  217-25     Citation Subset:  IM    
Affiliation:
Department of Laboratory Medicine, Hokkaido University Graduate School of Medicine, Kita-15, Nishi-7, Kita-ku, Sapporo 060-8638, Japan. kiizuka@med.hokudai.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Aorta / cytology,  drug effects*,  physiology
Atmospheric Pressure*
Cell Division / drug effects,  physiology
Cells, Cultured
Dose-Response Relationship, Drug
Growth Inhibitors / pharmacology*
Humans
Muscle, Smooth, Vascular / cytology,  drug effects*,  physiology
Propanolamines / pharmacology*
Chemical
Reg. No./Substance:
0/Growth Inhibitors; 0/Propanolamines; 81486-22-8/K 351

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