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JournalISSN: 1018-1172

Journal of Vascular Research 

Karger Publishers
About: Journal of Vascular Research is an academic journal published by Karger Publishers. The journal publishes majorly in the area(s): Vascular smooth muscle & Endothelium. It has an ISSN identifier of 1018-1172. Over the lifetime, 2288 publications have been published receiving 63624 citations. The journal is also known as: JVR.


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Journal ArticleDOI
TL;DR: Three common mutations in the 3′ untranslated region of the VEGF gene are found; one of them, a 936 C/T exchange, may be an important determinant of V EGF plasma levels.
Abstract: Background: Vascular endothelial growth factor (VEGF) is an important regulator of angiogenesis. Strong interindividual variations of VEGF plasma levels have been reported previousl

528 citations

Journal ArticleDOI
TL;DR: The ability of LY 83583 as well as hemoglobin to inhibit photorelaxation is consistent with the hypothesis that on radiation a photo-induced relaxing factor is formed which can stimulate guanylate cyclase and which can be inactivated by superoxide and by hemoglobin.
Abstract: The characteristics of carbon monoxide (CO)-induced, endothelium-independent relaxation of rabbit aorta were compared with those of nitric oxide (NO)-induced and light-induced relaxation and endotheli

506 citations

Journal ArticleDOI
William C. Sessa1
TL;DR: The purposes of this review are to highlight recent advances in the enzymology and molecular biology of this important family of proteins and to examine how this information pertains to the regulation of NO production.
Abstract: Nitric oxide (NO) is an important bio-regulatory molecule in the nervous, immune and cardiovascular systems. NO is synthesized from one of the guanidino nitrogens of L-arginine by the enzyme nitric oxide synthase (NOS). To date, several isoforms of NOS have been purified and cloned. These proteins represent a novel family of mammalian enzymes that contain both heme and cytochrome P450 reductase domains. The three prototypical forms of NOS: neuronal, cytokine-inducible and endothelial NOS, are derived from separate genes and are regulated by diverse signaling pathways. The purposes of this review are to highlight recent advances in the enzymology and molecular biology of this important family of proteins and to examine how this information pertains to the regulation of NO production.

472 citations

Journal ArticleDOI
TL;DR: Recent findings suggest that an imbalance in the production of NO and O2- within the vascular wall is one of the earliest events to occur in the atherogenic process.
Abstract: Endothelial injury or dysfunction has been proposed to be one of the initiating events of atherosclerosis and is associated with an apparent decrease in the production of the vasodilator autacoid nitr

437 citations

Journal ArticleDOI
TL;DR: This review will discuss wall shear stress in vivo, paying attention to its assessment and especially to the results obtained in both arterioles and large arteries, and the limitations of the methods currently in use.
Abstract: It has been well established that wall shear stress is an important determinant of endothelial cell function and gene expression as well as of its structure. There is increasing evidence that low wall shear stress, as present in artery bifurcations opposite to the flow divider where atherosclerotic lesions preferentially originate, expresses an atherogenic endothelial gene profile. Besides, wall shear stress regulates arterial diameter by modifying the release of vasoactive mediators by endothelial cells. Most of the studies on the influence of wall shear stress on endothelial cell function and structure have been performed in vitro, generally exposing endothelial cells from different vascular regions to an average wall shear stress level calculated according to Poiseuille's law, which does not hold for the in vivo situation, assuming wall shear stress to be constant along the arterial tree. Also in vivo wall shear stress has been determined based upon theory, assuming the velocity profile in arteries to be parabolic, which is generally not the case. Wall shear stress has been calculated, because of the lack of techniques to assess wall shear stress in vivo. In recent years, techniques have been developed to accurately assess velocity profiles in arterioles, using fluorescently labeled particles as flow tracers, and non-invasively in large arteries by means of ultrasound or magnetic resonance imaging. Wall shear rate is derived from the in vivo recorded velocity profiles and wall shear stress is estimated as the product of wall shear rate and plasma viscosity in arterioles and whole blood viscosity in large arteries. In this review, we will discuss wall shear stress in vivo, paying attention to its assessment and especially to the results obtained in both arterioles and large arteries. The limitations of the methods currently in use are discussed as well. The data obtained in the arterial system in vivo are compared with the theoretically predicted ones, and the consequences of values deviating from theory for in vitro studies are considered. Applications of wall shear stress as in flow-mediated arterial dilation, clinically in use to assess endothelial cell (dys)function, are also addressed. This review starts with some background considerations and some theoretical aspects.

415 citations

Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
20236
202235
202141
202038
201931
201833