Publications by authors named "T Suvorava"
Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) in the vessel wall regulates blood pressure and cardiovascular hemodynamics. In this study, we generated conditional eNOS knock out (KO) mice characterized by a duplicated/inverted exon 2 flanked with two pairs of loxP regions (eNOS); a Cre-recombinase activity induces cell-specific reactivation of eNOS, as a result of a flipping of the inverted exon 2 (eNOS). This work aimed to test the efficiency of the Cre-mediated cell-specific recombination and the resulting eNOS expression/function.
View Article and Find Full Text PDFAmong all physiologic functions of nitric oxide (NO) known so far, NO-dependent regulation of vascular tone is one of the most important. Under physiological conditions vascular NO is mainly generated by endothelial NO-synthase (eNOS), the major isoform of NOS in the cardiovascular system. NO produced in vascular endothelial cells displays complex physiologic activities considered to be vasoprotective.
View Article and Find Full Text PDFArticle Synopsis
- Red blood cells (RBCs) possess endothelial NO synthase (eNOS) and transport nitric oxide (NO), which is important for heart health, but the role of RBC eNOS in protecting the heart from damage is not well understood.
- Researchers used specially modified mice to differentiate between the functions of eNOS in RBCs and endothelial cells, discovering that RBC eNOS is crucial for limiting damage after heart attacks (acute myocardial infarction or AMI).
- While endothelial cell (EC) eNOS affects blood flow and heart function, RBC eNOS was found to specifically protect against heart tissue damage during AMI, suggesting it could be a viable target for new heart attack treatments.
Article Synopsis
- Arginase 1 (Arg1) is an enzyme that converts l-arginine into l-ornithine and urea, and its role in endothelial cells (ECs) may limit l-arginine availability for nitric oxide (NO) production, leading to vascular issues.
- A study was conducted using EC-specific gene-targeted knockout (KO) mice to examine how the absence of Arg1 affects eNOS, vascular tone, and endothelial function in normal conditions.
- Results showed that EC Arg1 KO mice maintained normal levels of l-arginine and NO, displayed preserved vascular relaxation, but had increased vasoconstriction response, suggesting that while Arg1 affects NO in specific organs, it does not majorly
Nitric Oxide Is the Cause of Nitroglycerin Tolerance: Providing an Old Dog New Tricks for Acute Heart Failure.
J Cardiovasc Pharmacol Ther
April 2022
Our paper highlights the past 50 years of research focusing solely on tolerance involving nitroglycerin (glyceryl trinitrate, GTN). It also identifies and discusses inconsistencies in previous mechanistic explanations that have failed to provide a way to administer GTN continuously, free of limitations from tolerance and without the requirement of a nitrate-free interval. We illustrate, for the first time in 135 years, a mechanism whereby nitric oxide, the mediator of vasodilation by GTN, may also be the cause of tolerance.
View Article and Find Full Text PDF