Document Detail


Colforsin-induced vasodilation in chronic hypoxic pulmonary hypertension in rats.
MedLine Citation:
PMID:  20300779     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE: Colforsin, a water-soluble forskolin derivative, directly activates adenylate cyclase and thereby increases the 3',5'-cyclic adenosine monophosphate (cAMP) level in vascular smooth muscle cells. In this study, we investigated the vasodilatory action of colforsin on structurally remodeled pulmonary arteries from rats with pulmonary hypertension (PH). METHODS: A total of 32 rats were subjected to hypobaric hypoxia (380 mmHg, 10% oxygen) for 10 days to induce chronic hypoxic PH, while 39 rats were kept in room air. Changes in isometric force were recorded in endothelium-intact (+E) and -denuded (-E) pulmonary arteries from the PH and control (non-PH) rats. RESULTS: Colforsin-induced vasodilation was impaired in both +E and -E arteries from PH rats compared with their respective controls. Endothelial removal did not influence colforsin-induced vasodilation in the arteries from control rats, but attenuated it in arteries from PH rats. The inhibition of nitric oxide (NO) synthase did not influence colforsin-induced vasodilation in +E arteries from controls, but attenuated it in +E arteries from PH rats, shifting its concentration-response curve closer to that of -E arteries from PH rats. Vasodilation induced by 8-bromo-cAMP (a cell-permeable cAMP analog) was also impaired in -E arteries from PH rats, but not in +E arteries from PH rats, compared with their respective controls. CONCLUSIONS: cAMP-mediated vasodilatory responses without beta-adrenergic receptor activation are impaired in structurally remodeled pulmonary arteries from PH rats. In these arteries, endothelial cells presumably play a compensatory role against the impaired cAMP-mediated vasodilatory response by releasing NO (and thereby attenuating the impairment). The results suggest that colforsin could be effective in the treatment of PH.
Authors:
Ayumu Yokochi; Hiroo Itoh; Junko Maruyama; Erquan Zhang; Baohua Jiang; Yoshihide Mitani; Chikuma Hamada; Kazuo Maruyama
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-03-19
Journal Detail:
Title:  Journal of anesthesia     Volume:  24     ISSN:  1438-8359     ISO Abbreviation:  J Anesth     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-06-14     Completed Date:  2010-09-10     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8905667     Medline TA:  J Anesth     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  432-40     Citation Subset:  IM    
Affiliation:
Department of Anesthesiology and Critical Care Medicine, Faculty of Medicine, University of Mie, 2-174 Edobashi, Tsu, Mie 514-8507, Japan. yokoti@clin.medic.mie-u.ac.jp
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MeSH Terms
Descriptor/Qualifier:
8-Bromo Cyclic Adenosine Monophosphate / pharmacology
Animals
Anoxia / drug therapy
Chronic Disease
Dinoprost / pharmacology
Drug Synergism
Fluorescent Dyes
Forskolin / analogs & derivatives*,  therapeutic use
Fura-2
Hypertension, Pulmonary / drug therapy*,  physiopathology
Hypertrophy, Right Ventricular / drug therapy,  physiopathology
Isometric Contraction / drug effects
Male
Muscle Contraction / drug effects
Potassium Chloride / pharmacology
Pulmonary Artery / drug effects
Rats
Rats, Wistar
Vasodilation / drug effects
Vasodilator Agents / therapeutic use*
Chemical
Reg. No./Substance:
0/Fluorescent Dyes; 0/Vasodilator Agents; 138605-00-2/colforsin; 23583-48-4/8-Bromo Cyclic Adenosine Monophosphate; 551-11-1/Dinoprost; 66428-89-5/Forskolin; 7447-40-7/Potassium Chloride; 96314-98-6/Fura-2

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