Effect of inhibition of nitric oxide synthesis on epicardial coronary artery caliber and coronary blood flow in humans

1994 ◽  
Vol 8 (1) ◽  
pp. 125
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Coronary Artery ◽  
Coronary Blood Flow ◽  
Nitric Oxide Synthesis ◽  
Epicardial Coronary Artery

scholarly journals Intracoronary Des-Acyl Ghrelin Acutely Increases Cardiac Perfusion Through a Nitric Oxide-Related Mechanism in Female Anesthetized Pigs

Endocrinology ◽  
2016 ◽  
Vol 157 (6) ◽  
pp. 2403-2415 ◽  
Author(s):  
Elena Grossini ◽  
Giulia Raina ◽  
Serena Farruggio ◽  
Lara Camillo ◽  
Claudio Molinari ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Endothelial Cells ◽  
Blood Flow ◽  
Coronary Artery ◽  
Coronary Blood Flow ◽  
No Synthase ◽  
Cardiac Perfusion ◽  
No Release ◽  
Acyl Ghrelin

Des-acyl ghrelin (DAG), the most abundant form of ghrelin in humans, has been found to reduce arterial blood pressure and prevent cardiac and endothelial cell apoptosis. Despite this, data regarding its direct effect on cardiac function and coronary blood flow, as well as the related involvement of autonomic nervous system and nitric oxide (NO), are scarce. We therefore examined these issues using both in vivo and in vitro studies. In 20 anesthetized pigs, intracoronary 100 pmol/mL DAG infusion with a constant heart rate and aortic blood pressure, increased coronary blood flow and NO release, whereas reducing coronary vascular resistances (P < .05). Dose responses to DAG were evaluated in five pigs. No effects on cardiac contractility/relaxation or myocardial oxygen consumption were observed. Moreover, whereas the blockade of muscarinic cholinoceptors (n = 5) or α- and β-adrenoceptors (n = 5 each) did not abolish the observed responses, NO synthase inhibition (n = 5) prevented the effects of DAG on coronary blood flow and NO release. In coronary artery endothelial cells, DAG dose dependently increased NO release through cAMP signaling and ERK1/2, Akt, and p38 MAPK involvement as well as the phosphorylation of endothelial NO synthase. In conclusion, in anesthetized pigs, DAG primarily increased cardiac perfusion through the involvement of NO release. Moreover, the phosphorylation of ERK1/2 and Akt appears to play roles in eliciting the observed NO production in coronary artery endothelial cells.

scholarly journals The human coronary vasodilatory response to acute mental stress is mediated by neuronal nitric oxide synthase

2017 ◽  
Vol 313 (3) ◽  
pp. H578-H583 ◽  
Author(s):  
Sitara G. Khan ◽  
Narbeh Melikian ◽  
Husain Shabeeh ◽  
Ana R. Cabaco ◽  
Katherine Martin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Coronary Artery ◽  
Nitric Oxide Synthase ◽  
Coronary Blood Flow ◽  
Mental Stress ◽  
Coronary Flow ◽  
Neuronal Nitric Oxide Synthase ◽  
Coronary Artery Diameter ◽  
Oxide Synthase

Mental stress-induced ischemia approximately doubles the risk of cardiac events in patients with coronary artery disease, yet the mechanisms underlying changes in coronary blood flow in response to mental stress are poorly characterized. Neuronal nitric oxide synthase (nNOS) regulates basal coronary blood flow in healthy humans and mediates mental stress-induced vasodilation in the forearm. However, its possible role in mental stress-induced increases in coronary blood flow is unknown. We studied 11 patients (6 men and 5 women, mean age: 58 ± 14 yr) undergoing elective diagnostic cardiac catheterization and assessed the vasodilator response to mental stress elicited by the Stroop color-word test. Intracoronary substance P (20 pmol/min) and isosorbide dinitrate (1 mg) were used to assess endothelium-dependent and -independent vasodilation, respectively. Coronary blood flow was estimated using intracoronary Doppler recordings and quantitative coronary angiography to measure coronary artery diameter. Mental stress increased coronary flow by 34 ± 7.0% over the preceding baseline during saline infusion ( P < 0.01), and this was reduced to 26 ± 7.0% in the presence of the selective nNOS inhibitor S-methyl-l-thiocitrulline (0.625 µmol/min, P < 0.001). Mental stress increased coronary artery diameter by 6.9 ± 3.7% ( P = 0.02) and 0.5 ± 2.8% ( P = 0.51) in the presence of S-methyl-l-thiocitrulline. The response to substance P did not predict the response to mental stress ( r2 = −0.22, P = 0.83). nNOS mediates the human coronary vasodilator response to mental stress, predominantly through actions at the level of coronary resistance vessels. NEW & NOTEWORTHY Acute mental stress induces vasodilation of the coronary microvasculature. Here, we show that this response involves neuronal nitric oxide synthase in the human coronary circulation. Listen to this article’s corresponding podcast at http://ajpheart.podbean.com/e/nnos-and-coronary-flow-during-mental-stress/ .

Reactive dilation and late-hyperemic constriction of epicardial coronary artery after short coronary occlusion

1986 ◽  
Vol 251 (3) ◽  
pp. H554-H561
Author(s):  
H. Yamamoto ◽  
H. Tomoike ◽  
K. Hisano ◽  
T. Inoue ◽  
M. Mohri ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Coronary Blood Flow ◽  
Coronary Occlusion ◽  
Reactive Hyperemia ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Epicardial Coronary Artery ◽  
Dependent Change ◽  
Coronary Artery Diameter

Coronary blood flow and epicardial coronary artery diameter were simultaneously measured by an electromagnetic or Doppler flow probe and a pair of ultrasonic crystals, respectively, during reactive hyperemia in conscious dogs. Reactive dilation appeared after the full appearance of reactive hyperemia and lasted for a period of 4-20 times the duration of the coronary occlusion. beta-Receptor blockade (propranolol, 1 mg/kg iv) attenuated both the reactive hyperemia in volume by 21-22% (P less than 0.01) and dilative responses of the epicardial coronary diameter by 27-28% (P less than 0.01), despite a nonsignificant attenuation of the resting or peak hyperemic coronary blood flow. When coronary blood flow was held constant during reperfusion, by an occluder distal to the ultrasonic crystals, the reactive dilation disappeared. A peculiar reactive constriction was noted when coronary occlusion was performed proximal to the site of the ultrasonic crystals. Appearance of this constriction was at 149 and 385 s after the release of 5 and 60 s of coronary occlusion, respectively. This late reactive constriction disappeared after pretreatment with alpha- (phentolamine, 1 mg/kg iv) and/or alpha- + beta-blockade, but not with beta-blockade alone, and it was not observed when the coronary diameter was measured proximal to the occluder. Thus reactive dilation of the epicardial coronary artery derives from an increase in coronary flow and is reduced by propranolol via a reduction in the hyperemic flow, suggesting a flow-dependent change in the diameter of the epicardial coronary artery. Reactive constriction is a local phenomenon following marked reduction in the coronary diameter and is abolished by alpha-adrenergic blockade with phentolamine.

scholarly journals Magnesium causes nitric oxide independent coronary artery vasodilation in humans

Heart ◽  
2001 ◽  
Vol 86 (2) ◽  
pp. 212-216
Author(s):  
H Teragawa ◽  
M Kato ◽  
T Yamagata ◽  
H Matsuura ◽  
G Kajiyama
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Coronary Artery ◽  
Coronary Blood Flow ◽  
Coronary Arteries ◽  
Quantitative Coronary Angiography ◽  
University Hospital ◽  
Nitric Oxide Synthase Inhibitor ◽  
Before And After ◽  
Synthase Inhibitor

OBJECTIVETo determine how magnesium affects human coronary arteries and whether endothelium derived nitric oxide (EDNO) is involved in the coronary arterial response to magnesium.DESIGNQuantitative coronary angiography and Doppler flow velocity measurements were used to determine the effects of the nitric oxide synthase inhibitorNG-monomethyl-L-arginine (L-NMMA) on magnesium induced dilation of the epicardial and resistance coronary arteries.SETTINGHiroshima University Hospital a tertiary cardiology centre.PATIENTS17 patients with angiographically normal coronary arteries.INTERVENTIONSMagnesium sulfate (MgSO4) (0.02 mmol/min and 0.2 mmol/min) was infused for two minutes into the left coronary ostium before and after intracoronary infusion of L-NMMA.MAIN OUTCOME MEASURESDiameter of the proximal and distal segments of the epicardial coronary arteries and coronary blood flow.RESULTSAt a dose of 0.02 mmol/min, MgSO4 did not affect the coronary arteries. At a dose of 0.2 mmol/min, MgSO4 caused coronary artery dilation (mean (SEM) proximal diameter 3.00 (0.09) to 3.11 (0.09) mm; distal 1.64 (0.06) to 1.77 (0.07) mm) and increased coronary blood flow (79.3 (7.5) to 101.4 (9.9) ml/min, p < 0.001 vbaseline for all). MgSO4 increased the changes in these parameters after the infusion of L-NMMA (p < 0.001v baseline).CONCLUSIONSMagnesium dilates both the epicardial and resistance coronary arteries in humans. Furthermore, the coronary arterial response to magnesium is dose dependent and independent of EDNO.

KATP + channels, nitric oxide, and adenosine are not required for local metabolic coronary vasodilation

2001 ◽  
Vol 280 (2) ◽  
pp. H868-H875 ◽  
Author(s):  
Johnathan D. Tune ◽  
Keith Neu Richmond ◽  
Mark W. Gorman ◽  
Eric O. Feigl
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Oxygen Tension ◽  
Adenosine Receptors ◽  
Myocardial Oxygen Consumption ◽  
Nitric Oxide Synthesis ◽  
Coronary Vasodilation ◽  
Adenosine Concentration

The role of ATP-sensitive K+ (KATP +) channels, nitric oxide, and adenosine in coronary exercise hyperemia was investigated. Dogs ( n = 10) were chronically instrumented with catheters in the aorta and coronary sinus and instrumented with a flow transducer on the circumflex coronary artery. Cardiac interstitial adenosine concentration was estimated from arterial and coronary venous plasma concentrations using a previously tested mathematical model. Experiments were conducted at rest and during graded treadmill exercise with and without combined inhibition of KATP + channels (glibenclamide, 1 mg/kg iv), nitric oxide synthesis ( N ω-nitro-l-arginine, 35 mg/kg iv), and adenosine receptors (8-phenyltheophylline, 3 mg/kg iv). During control exercise, myocardial oxygen consumption increased ∼2.9-fold, coronary blood flow increased ∼2.6-fold, and coronary venous oxygen tension decreased from 19.9 ± 0.4 to 13.7 ± 0.6 mmHg. Triple blockade did not significantly change the myocardial oxygen consumption or coronary blood flow response during exercise but lowered the resting coronary venous oxygen tension to 10.0 ± 0.4 mmHg and during exercise to 6.2 ± 0.5 mmHg. Cardiac adenosine levels did not increase sufficiently to overcome the adenosine receptor blockade. These results indicate that combined inhibition of KATP + channels, nitric oxide synthesis, and adenosine receptors lowers the balance between total oxygen supply and consumption at rest but that these factors are not required for local metabolic coronary vasodilation during exercise.

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