Effects of nitric oxide inhibition on basal forearm blood flow in patients with nonischemic chronic heart failure

1998 ◽  
Vol 13 (3) ◽  
pp. 142-146 ◽  
Author(s):  
Hiroaki Yoshida ◽  
Motoyuki Nakamura ◽  
Tomonari Akatsu ◽  
Naoshi Arakawa ◽  
Katsuhiko Hiramori
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Blood Flow ◽  
Chronic Heart Failure ◽  
Forearm Blood Flow ◽  
Nitric Oxide Inhibition ◽  
Oxide Inhibition

Effect of endothelin-1 on endothelium-derived vascular responsiveness in man

1998 ◽  
Vol 95 (2) ◽  
pp. 151-156 ◽  
Author(s):  
Henry KRUM ◽  
Noel CRANSWICK ◽  
Anne-Marie PELLIZZER
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Blood Flow ◽  
Chronic Heart Failure ◽  
Brachial Artery ◽  
Forearm Blood Flow ◽  
Nitric Oxide Production ◽  
Reactive Hyperaemia ◽  
Endothelin 1 ◽  
Oxide Production

1.Endothelium-dependent vasodilatation via nitric oxide in response to muscarinic stimulation is decreased in chronic heart failure while basal release of nitric oxide may be increased. As production of the endothelium-derived vasoconstrictor endothelin-1 is increased in chronic heart failure, endothelin-1 may act in an autocrine manner to modulate these effects. 2.To test this, we determined whether prolonged endothelin infusion in normal subjects would reproduce the alterations in basal and stimulated nitric oxide release observed in patients with chronic heart failure. Basal nitric oxide production was determined by measurement of forearm blood flow using strain gauge venous occlusion plethysmography before and after brachial artery infusion of a nitric oxide synthase inhibitor (NG-monomethyl-l-arginine). Stimulated nitric oxide production was determined by brachial artery infusion of acetylcholine. As metabolic vasodilatation is thought to be mediated in part via nitric oxide and is decreased in chronic heart failure, forearm blood flow during peak reactive hyperaemia was also measured. Studies were then repeated during brachial artery infusion of endothelin-1 and a non-specific vasoconstrictor, noradrenaline. 3.Neither basal nor stimulated nitric oxide production was altered by endothelin-1 and noradrenaline infusion. However, absolute forearm blood flow responses to peak reactive hyperaemia were decreased during infusion of endothelin-1 in comparison to noradrenaline. These data suggest that increased endothelin-1 may not contribute greatly to altered basal and stimulated nitric oxide production in patients with chronic heart failure but may contribute to impaired metabolic vasodilatation, by mechanisms presumably unrelated to altered nitric oxide production.

scholarly journals Nitric Oxide Inhibition Impairs Blood Flow During Exercise in Hearts With a Collateral-Dependent Myocardial Region

1998 ◽  
Vol 31 (1) ◽  
pp. 67-74 ◽  
Author(s):  
Jay H Traverse ◽  
James W Kinn ◽  
Christopher Klassen ◽  
Dirk J Duncker ◽  
Robert J Bache
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Inhibition ◽  
Oxide Inhibition

NITRIC OXIDE INHIBITION IN AN OVINE MODEL OF HEART FAILURE

1996 ◽  
Vol 23 (5) ◽  
pp. 403-409 ◽  
Author(s):  
Miriam Tessa Rademaker ◽  
Michael Andrew Fitzpatrick ◽  
Arthur Mark Richards ◽  
Michael Gary Nicholls ◽  
Christopher John Charles ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Ovine Model ◽  
Nitric Oxide Inhibition ◽  
Oxide Inhibition

Effect of chronic renal medullary nitric oxide inhibition on blood pressure

1994 ◽  
Vol 266 (5) ◽  
pp. H1918-H1926 ◽  
Author(s):  
D. L. Mattson ◽  
S. Lu ◽  
K. Nakanishi ◽  
P. E. Papanek ◽  
A. W. Cowley
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Renal Medulla ◽  
Sodium Balance ◽  
Sprague Dawley ◽  
Nitric Oxide Inhibition ◽  
Medullary Blood Flow ◽  
Nitric Oxide Inhibitor ◽  
Oxide Inhibition

The effects of chronic nitric oxide inhibition in the renal medulla on renal cortical and medullary blood flow, sodium balance, and blood pressure were evaluated in conscious uninephrectomized Sprague-Dawley rats. During a 5-day renal medullary interstitial infusion of the nitric oxide inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 120 micrograms/h) in saline (0.5 ml/min), renal medullary blood flow was selectively decreased by 30% after 2 h and was maintained at that level for the entire infusion. The decrease in medullary blood flow was associated with sodium retention and increased blood pressure. After the cessation of L-NAME infusion, medullary blood flow returned to control, and the sodium balance became negative as blood pressure returned to baseline. These data indicate that renal medullary nitric oxide plays an important role in the regulation of renal blood flow, sodium excretion, and blood pressure.

scholarly journals Influence of Chronic Nitric Oxide Inhibition of Coronary Blood Flow Regulation

1998 ◽  
Vol 62 (5) ◽  
pp. 371-378 ◽  
Author(s):  
Shinji Tayama ◽  
Ken Okumura ◽  
Toshiro Matsunaga ◽  
Ryusuke Tsunoda ◽  
Toshifumi Tabuchi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Coronary Blood Flow ◽  
Flow Regulation ◽  
Nitric Oxide Inhibition ◽  
Blood Flow Regulation ◽  
Oxide Inhibition
Sign in / Sign up

Export Citation Format

Share Document