This publication is protected and can be accessed only from certain IPs.
This publication is protected and can be accessed only from certain IPs.

Title: Coronary endothelial dysfunction in heart failure in Tgαq*44 mice


Endothelial dysfunction (ED) is a hallmark of heart failure (HF). Clinically, most cases of HF is due to CAD. On the other hand, ED is seen in patient with severe HF of non-ischemic origin. Mechanisms leading to the development of secondary type of ED are still not clear. Aim of the present study was to describe the development of secondary type of coronary ED in Tgαq*44 mice as well as to elucidate the involvement of aldosterone in this phenomenon. Both coronary endothelium-dependent and endothelium-independent responses were assessed in isolated Tgαq*44 hearts and age-matched FVB mice. In addition, level of 6-keto-PGF1α in cardiac effluent and production of 02- in cardiac tissue were assessed. Despite increased generation of O2- in cardiac tissue, endothelial function was not altered in Tgαq*44 mice at the age of 4 months. However, coronary ED developed, as evidenced by impaired NO-induced but not PGI2-induced vasodilatation in Tgαq*44 mice at the age of 14 months. Interestingly, there was a compensatory increase in basal PGI2 production in Tgαq*44 hearts. Treatment of Tgαq*44 mice with canrenone, aldosteron receptor antagonist improved both survival and NO-mediated vasodilatation in Tgαq*44 mice but had no effects on heart hypertrophy, pulmonary congestion and basal PGI2 production. In conclusion, development of coronary ED is secondary to cardiomyocytes pathology in T ; gαq*44 mice and is characterized by decreased NO bioavailability and compensatory increase in PGI2 production in coronary circulation. Development of secondary type of coronary ED in Tgαq*44 mice is at last partly related to aldosterone in Tgαq*44 mice.

Place of publishing:


Level of degree:

2 - studia doktoranckie

Degree discipline:

choroby układu krążenia

Degree grantor:

Wydział Lekarski


Chłopicki, Stefan

Date issued:




Call number:




Access rights:

tylko w bibliotece

Object collections:

Last modified:

Feb 3, 2023

In our library since:

Jun 27, 2022

Number of object content hits:


Number of object content views in PDF format


All available object's versions:


Show description in RDF format:


Show description in OAI-PMH format:


Edition name Date
ZB-104209 Feb 3, 2023


Citation style:

This page uses 'cookies'. More information