Oxidations ofNω-Hydroxyarginine Analogues and VariousN-Hydroxyguanidines by NO Synthase II: Key Role of Tetrahydrobiopterin in the Reaction Mechanism and Substrate Selectivity

2001 ◽  
Vol 14 (2) ◽  
pp. 202-210 ◽  
Author(s):  
Catherine Moali ◽  
Jean-Luc Boucher ◽  
Axelle Renodon-Corniere ◽  
Dennis J. Stuehr ◽  
Daniel Mansuy
Keyword(s):  
Reaction Mechanism ◽  
No Synthase ◽  
Substrate Selectivity

Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

1994 ◽  
Vol 267 (1) ◽  
pp. R84-R88 ◽  
Author(s):  
M. Huang ◽  
M. L. Leblanc ◽  
R. L. Hester
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Cardiac Output ◽  
No Synthase ◽  
Before And After ◽  
Regional Hemodynamics ◽  
Autonomic Blockade ◽  
Infusion Of Norepinephrine ◽  
Oxide Synthase

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.

scholarly journals Role of Neural NO Synthase (nNOS) Uncoupling in the Dysfunctional Nitrergic Vasorelaxation of Penile Arteries from Insulin-Resistant Obese Zucker Rats

PLoS ONE ◽  
2012 ◽  
Vol 7 (4) ◽  
pp. e36027 ◽  
Author(s):  
Ana Sánchez ◽  
Cristina Contreras ◽  
María Pilar Martínez ◽  
Belén Climent ◽  
Sara Benedito ◽  
...  
Keyword(s):  
No Synthase ◽  
Zucker Rats ◽  
Insulin Resistant ◽  
Obese Zucker Rats ◽  
Penile Arteries

scholarly journals The Important Role of Halogen Bond in Substrate Selectivity of Enzymatic Catalysis

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Shuiqin Jiang ◽  
Lujia Zhang ◽  
Dongbin Cui ◽  
Zhiqiang Yao ◽  
Bei Gao ◽  
...  
Keyword(s):  
Halogen Bond ◽  
Enzymatic Catalysis ◽  
Substrate Selectivity

Contractions induced by NO synthase inhibition in isolated rat basilar artery: Role of the endothelium and endogeneous vasoconstrictors

1998 ◽  
Vol 20 (1) ◽  
pp. 63-72 ◽  
Author(s):  
Ralf Hempelmann ◽  
Rainer Prade ◽  
Maximilian Mehdorn ◽  
Albrecht Ziegler
Keyword(s):  
Basilar Artery ◽  
No Synthase ◽  
Isolated Rat

Reaction Mechanism and Role of the Support in the Partial Oxidation of Methane on Rh/Al2O3

1996 ◽  
Vol 159 (2) ◽  
pp. 418-426 ◽  
Author(s):  
Dezheng Wang ◽  
Olivier Dewaele ◽  
Ann M.De Groote ◽  
Gilbert F. Froment
Keyword(s):  
Reaction Mechanism ◽  
Partial Oxidation ◽  
Partial Oxidation Of Methane ◽  
Oxidation Of Methane

Increased coronary perfusion augments cardiac contractility in the rat through stretch-activated ion channels

2002 ◽  
Vol 282 (4) ◽  
pp. H1334-H1340 ◽  
Author(s):  
R. R. Lamberts ◽  
M. H. P. van Rijen ◽  
P. Sipkema ◽  
P. Fransen ◽  
S. U. Sys ◽  
...  
Keyword(s):  
Ion Channels ◽  
Perfusion Pressure ◽  
Cardiac Contractility ◽  
No Synthase ◽  
Coronary Perfusion ◽  
Channel Blockade ◽  
No Release ◽  
Sustained Increase ◽  
Stretch Activated Ion Channels

The role of stretch-activated ion channels (SACs) in coronary perfusion-induced increase in cardiac contractility was investigated in isolated isometrically contracting perfused papillary muscles from Wistar rats. A brief increase in perfusion pressure (3–4 s, perfusion pulse, n = 7), 10 repetitive perfusion pulses ( n = 4), or a sustained increase in perfusion pressure (150–200 s, perfusion step, n = 7) increase developed force by 2.7 ± 1.1, 7.7 ± 2.2, and 8.3 ± 2.5 mN/mm2 (means ± SE, P < 0.05), respectively. The increase in developed force after a perfusion pulse is transient, whereas developed force during a perfusion step remains increased by 5.1 ± 2.5 mN/mm2 ( P < 0.05) in the steady state. Inhibition of SACs by addition of gadolinium (10 μmol/l) or streptomycin (40 and 100 μmol/l) blunts the perfusion-induced increase in developed force. Incubation with 100 μmol/l N ω-nitro-l-arginine [nitric oxide (NO) synthase inhibition], 10 μmol/l sodium nitroprusside (NO donation) and 0.1 μmol/l verapamil (L-type Ca2+ channel blockade) are without effect on the perfusion-induced increase of developed force. We conclude that brief, repetitive, or sustained increases in coronary perfusion augment cardiac contractility through activation of stretch-activated ion channels, whereas endothelial NO release and L-type Ca2+channels are not involved.

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