Is NO the king? Pathophysiological benefit with uncertain clinical impact

Title:

Is NO the king? Pathophysiological benefit with uncertain clinical impact

Creator:

Fedor Šimko

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:a975ed42-1911-4ff4-9cab-bd23e17a950b
uuid:a975ed42-1911-4ff4-9cab-bd23e17a950b
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, fyziologie, nitric oxide, physiology, NO donor, cardiovascular mortality, clinical trial, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

NO is the “hero” molecule of the last few decades. It is a ubiquitous and omnipotent radical with both hemodynamic and antiproliferative effects within the cardiovascular system. NO is an important counterregulatory factor for vasoconstrictors and growth promoting substances. Endothelial dysfunction with decreased NO production is related to many cardiovascular disorders, such as coronary artery disease, heart failure and hypertension. Despite the important role of NO within the circulation, there is only limited evidence in the form of large clinical trials that NO delivery can reduce cardiovascular morbidity and mortality. Thus, NO donors are not in the first line therapy in ischemic heart disease, heart failure or arterial hypertension and NO delivery is recommended only in particular clinical situations, when a well established treatment is contraindicated or has an insufficient effect. It is concluded that the insufficient NO production is the principal disorder in endothelial dysfunction, which is related to cardiovascular pathology with deteriorated prognosis, but the impact of therapeutically increased NO bioactivity on the morbidity and mortality is inferior to well established treatment with ACE-inhibitors, AT1 receptor blockers, beta-blockers, statins and certain antihypertensive drugs. There is little doubt that NO is king in the circulation, but kings seldom decide the battles., Fedor Šimko., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2007 Volume:56 | Number:Suppl 2

Harvested from:

CDK

Metadata only:

false