Document Detail

Myosin isoform shifts and decreased reactivity in hypoxia-induced hypertensive pulmonary arterial muscle.
MedLine Citation:
PMID:  9612293     Owner:  NLM     Status:  MEDLINE    
The principal stimulus that evokes pulmonary hypertension is chronic alveolar hypoxia. Pulmonary hypertension is associated with remodeling of the vessel walls, involving hypertrophy and hyperplasia of pulmonary arterial smooth muscle (PASM) and a concomitant increase in the deposition of connective tissue, resulting in increased wall thickness. The purpose of the present study was to determine the effect of hypoxia-induced hypertension on the structure and function of PASM. Experiments were designed to determine whether hypoxia-induced pulmonary hypertension is associated with alterations in PASM: 1) reactivity to a variety of agonists, 2) contractile protein proportions and isoforms, and 3) structural properties. Young adult male rats were made hypoxic by lowering the fraction of inspired O2 (10%) for 14 days. Pulmonary arterial segments were isolated and dose-response curves to various agonists (high K+, norepinephrine, serotonin, angiotensin II, and adenosine) were generated. Gel electrophoresis was used to measure changes in the relative amounts of actin or myosin and of myosin heavy chain (MHC) isoforms. Structural changes were correlated with the pharmacological and biochemical data. Hypoxia-induced pulmonary hypertension caused a general decreased reactivity, an increase in the proportion of nonmuscle to muscle MHC isoforms in PASM, and an increase in arterial wall thickness with PASM hypertrophy or hyperplasia.
C S Packer; J E Roepke; N H Oberlies; R A Rhoades
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  274     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1998 May 
Date Detail:
Created Date:  1998-07-01     Completed Date:  1998-07-01     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  L775-85     Citation Subset:  IM    
Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis 46202, USA.
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MeSH Terms
Adenosine / pharmacology
Angiotensin II / pharmacology
Anoxia / complications*
Dose-Response Relationship, Drug
Hypertension / enzymology*,  etiology*,  pathology
Muscle, Smooth, Vascular / drug effects,  enzymology*,  pathology
Myosins / metabolism*
Norepinephrine / pharmacology
Potassium / pharmacology
Pulmonary Artery / drug effects,  enzymology*,  pathology
Rats, Sprague-Dawley
Serotonin / pharmacology
Grant Support
Reg. No./Substance:
11128-99-7/Angiotensin II; 50-67-9/Serotonin; 51-41-2/Norepinephrine; 58-61-7/Adenosine; 7440-09-7/Potassium; EC

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