scholarly journals The Retinal Relaxing Factor: Update on an Enigmatic Regulator of the Retinal Circulation

2017 ◽  
Vol 58 (3) ◽  
pp. 1702 ◽  
Author(s):  
Laura Vanden Daele ◽  
Charlotte Boydens ◽  
Bart Pauwels ◽  
Johan Van de Voorde
Keyword(s):  
Retinal Circulation ◽  
Relaxing Factor

The response of the retinal circulation to altitude

1971 ◽  
Vol 127 (4) ◽  
pp. 708-711 ◽  
Author(s):  
R. Frayser
Keyword(s):  
Retinal Circulation

Retinal circulation times in branch retinal vein occlusion

1995 ◽  
Vol 9 (2) ◽  
pp. 107 ◽  
Author(s):  
Gumin Kang ◽  
Jaeheung Lee
Keyword(s):  
Retinal Vein Occlusion ◽  
Branch Retinal Vein Occlusion ◽  
Retinal Circulation ◽  
Vein Occlusion

Why is a new journal dedicated to vascular biology required?

2018 ◽  
Author(s):  
Paolo Madeddu
Keyword(s):  
Myocardial Ischemia ◽  
Tumor Growth ◽  
Vascular Tone ◽  
50Th Anniversary ◽  
Vascular Biology ◽  
Active Process ◽  
Master Regulators ◽  
Relaxing Factor ◽  
Tissue Healing ◽  
Endothelium Derived Relaxing Factor

The year 2018 marked the 110th anniversary of Goldmann’s discovery that vascularization is an active process in tissues1 and the 50th anniversary of the concomitant reports from Greenblatt and Shubik2 and Ehrmann and Knoth3 that soluble morphogenic factors are required for cancer angiogenesis. Many other radically transformative paradigms have been introduced in the last decades. To name a few, the molecular search for the identity of master regulators of vascular tone led to the discovery of the Endothelium-Derived Relaxing Factor (EDRF; i.e., NO4), while clinically inspired investigations led to the recognition of the pathophysiological relevance of neoangiogenesis in cancer and tissue healing. This brought about the proposal of blocking angiogenesis to halt tumor growth and stimulating angiogenesis to treat myocardial ischemia and heart failure5-7.

Modulation of cerebral arterial tone by endothelium-derived relaxing factor

1993 ◽  
Vol 264 (4) ◽  
pp. H1245-H1250 ◽  
Author(s):  
J. E. Brian ◽  
R. H. Kennedy
Keyword(s):  
Nitric Oxide ◽  
Muscle Tone ◽  
Cerebral Arteries ◽  
Maximum Tension ◽  
Relaxing Factor ◽  
Middle Cerebral Arteries ◽  
Endothelium Derived Relaxing Factor ◽  
Vascular Smooth Muscle Tone ◽  
Dose Dependent ◽  
Arterial Tone

This study was designed to further elucidate the role of the endothelium in regulation of cerebral vascular smooth muscle tone. Dose-dependent vasoconstrictive effects of serotonin (5-HT) were examined in endothelium-intact and endothelium-denuded ring segments prepared from canine basilar and middle cerebral arteries. Some preparations were pretreated with 10(-5) M N omega-nitro-L-arginine (L-NNA), an agent that inhibits the production of L-arginine-derived nitric oxide, one of the compounds proposed to be endothelium-derived relaxing factor. L-NNA alone elicited marked dose-dependent increases in tension in endothelium-intact preparations; a significantly smaller response was seen in endothelium-denuded preparations. The effects of L-NNA on endothelium-intact preparations were partially reversed by washing and treatment with L-arginine. The maximum tension induced by 5-HT was approximately doubled by removal of the endothelium as well as by L-NNA treatment of endothelium-intact preparations; a slight increase in maximum tension occurred in endothelium-denuded preparations treated with L-NNA. The concentration of 5-HT producing half-maximal contraction (ED50) was not affected by L-NNA. These data suggest that L-arginine-derived nitric oxide modulates canine cerebral arterial tone in both the resting state and during contraction with 5-HT.

scholarly journals Cloning and expression of a cDNA encoding human endothelium-derived relaxing factor/nitric oxide synthase.

1992 ◽  
Vol 267 (21) ◽  
pp. 14519-14522
Author(s):  
S.P. Janssens ◽  
A Shimouchi ◽  
T Quertermous ◽  
D.B. Bloch ◽  
K.D. Bloch
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cloning And Expression ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Oxide Synthase ◽  
Human Endothelium

Endothelial Dysfunction in Shock States

Physiology ◽  
1993 ◽  
Vol 8 (4) ◽  
pp. 145-148 ◽  
Author(s):  
AGB Kovach ◽  
AM Lefer
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Tissue Injury ◽  
Circulatory Shock ◽  
Relaxing Factor ◽  
Vascular Beds ◽  
Endothelium Derived Relaxing Factor

Circulatory shock results in dysfunction of the endothelium in various vascular beds. This dysfunction is characterized by marked impairment in the vasculature's ability to relax to endothelium-dependent vasodilators. This loss of endothelium-derived relaxing factor, or nitric oxide, leads to profound tissue injury.

Acute compensation to abrupt occlusion of rat femoral artery is prevented by NO synthase inhibitors

1994 ◽  
Vol 267 (6) ◽  
pp. H2523-H2530 ◽  
Author(s):  
J. L. Unthank ◽  
J. C. Nixon ◽  
M. C. Dalsing
Keyword(s):  
Femoral Artery ◽  
Arterial Occlusion ◽  
Artery Occlusion ◽  
No Synthase ◽  
Artery Blood Flow ◽  
Relaxing Factor ◽  
Femoral Artery Occlusion ◽  
Before And After ◽  
Endothelium Derived Relaxing Factor ◽  
Oxide Synthase

The hemodynamic significance of endothelium-derived relaxing factor (EDRF)-mediated mechanisms in vascular responses to abrupt rat femoral artery occlusion was investigated. Temporary arterial occlusion was produced before and after inhibition of nitric oxide synthase by N omega-nitro-L-arginine methyl ester (L-NAME) or NG-monomethyl-L-arginine (L-NMMA). Iliac artery blood flow and arterial pressures proximal and distal to the occlusion were measured. Normal vascular compensation included a return of resistance to preocclusion levels and a rise in distal pressure to a plateau within 5 min postocclusion. After treatment with L-NAME and L-NMMA, postocclusion resistance remained elevated by 53 and 36%, respectively. Collateral dilation after occlusion, as indicated by the rise in distal pressure, was prevented by L-NAME but not L-NMMA. Increases in adrenergic tone and mean arterial pressure by phenylephrine did not prevent compensation, suggesting the effects of L-NAME and L-NMMA did not result from elevated sympathetic activation or pressure. The results are consistent with the hypothesis that the stimulated release of endothelium-derived relaxing factor mediates the acute vascular compensation to abrupt arterial occlusion.

scholarly journals Inhibition by l-glutamine of the release of endothelium-derived relaxing factor from cultured endothelial cells

1990 ◽  
Vol 101 (2) ◽  
pp. 237-239 ◽  
Author(s):  
Markus Hecker ◽  
Jane A. Mitchell ◽  
Tomasz A. Swierkosz ◽  
William C. Sessa ◽  
John R. Vane
Keyword(s):  
Endothelial Cells ◽  
Relaxing Factor ◽  
Cultured Endothelial Cells ◽  
Endothelium Derived Relaxing Factor
Sign in / Sign up

Export Citation Format

Share Document