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

• Published in: Bulletin of experimental biology and medicine Vol. 169; no. 3; pp. 314 - 317
• Main Author: Davydova, M. P.
• Format: Journal Article
• Language: English
• 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
• ISSN: 0007-4888; 1573-8221
• DOI: 10.1007/s10517-020-04877-8

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.