Modeling of Hypervolemia in Pulmonary Circulation in Rats Changes the Structure of NO-Mediated Relaxation of Pulmonary Arteries

We analyzed the contribution of soluble guanylate cyclase-dependent pathway into NO-mediated relaxation of pulmonary arteries under conditions of high pulmonary blood flow modeled by creation of carotid artery-jugular vein shunt in rats. Inhibitor of soluble guanylate cyclase suppressed NO-donor ind...

Full description

Saved in:
Bibliographic Details
Published inBulletin of experimental biology and medicine Vol. 169; no. 3; pp. 314 - 317
Main Author Davydova, M. P.
Format Journal Article
LanguageEnglish
Published New York Springer US 01.07.2020
Springer
Subjects
Arteries
Biomedical and Life Sciences
Biomedicine
Blood vessels
Cell Biology
Dilatation
Internal Medicine
Laboratory Medicine
Nitric oxide
Pathology
Sapropterin dihydrochloride
nitric oxide
pulmonary artery
soluble guanylate cyclase
carotid artery-jugular vein shunt
Online AccessGet full text

Cover

More Information
Summary:We analyzed the contribution of soluble guanylate cyclase-dependent pathway into NO-mediated relaxation of pulmonary arteries under conditions of high pulmonary blood flow modeled by creation of carotid artery-jugular vein shunt in rats. Inhibitor of soluble guanylate cyclase suppressed NO-donor induced relaxation was lower in rats with shunt, but dilatation in response to phosphodiesterase V inhibitor did not differ in the sham-operated and shunt groups. Thus, the structure of NO-mediated vasodilatation of pulmonary arteries under conditions of hypervolemia of pulmonary circulation was shifted to soluble guanylate cyclase-independent pathways, whereas intracellular soluble guanylate cyclase-dependent mechanisms of dilatation were in general unchanged.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0007-4888
1573-8221
DOI:10.1007/s10517-020-04877-8