ACE Inhibitors Promote Nitric Oxide Accumulation to Modulate Myocardial Oxygen Consumption

Circulation ◽  
1997 ◽  
Vol 95 (1) ◽  
pp. 176-182 ◽  
Author(s):  
Xiaoping Zhang ◽  
Yi-Wu Xie ◽  
Alberto Nasjletti ◽  
Xiaobin Xu ◽  
Michael S. Wolin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Ace Inhibitors ◽  
Myocardial Oxygen Consumption

scholarly journals NO modulates myocardial O2consumption in the nonhuman primate: an additional mechanism of action of amlodipine

1999 ◽  
Vol 276 (6) ◽  
pp. H2069-H2075 ◽  
Author(s):  
Paul R. Forfia ◽  
Xiaoping Zhang ◽  
Delvin R. Knight ◽  
Andrew H. Smith ◽  
Christopher P. A. Doe ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Nonhuman Primate ◽  
Myocardial Oxygen Consumption ◽  
Channel Blocker ◽  
Tissue Response ◽  
Canine Heart ◽  
Additional Mechanism

Recent evidence from our laboratory and others suggests that nitric oxide (NO) is a modulator of in vivo and in vitro oxygen consumption in the murine and canine heart. Therefore, the goal of our study was twofold: to determine whether NO modulates myocardial oxygen consumption in the nonhuman primate heart in vitro and to evaluate whether the seemingly cardioprotective actions of amlodipine may involve an NO-mediated mechanism. Using a Clark-type O2 electrode, we measured oxygen consumption in cynomologous monkey heart at baseline and after increasing doses of S-nitroso- N-acetylpenicillamine (SNAP; 10−7–10−4M), bradykinin (10−7–10−4M), ramiprilat (10−7–10−4M), and amlodipine (10−7–10−5M). SNAP (−38 ± 5.8%), bradykinin (−19 ± 3.9%), ramiprilat (−28 ± 2.3%), and amlodipine (−23 ± 4.5%) each caused significant ( P < 0.05) reductions in myocardial oxygen consumption at their highest dose. Preincubation of tissue with nitro-l-arginine methyl ester (10−4 M) blunted the effects of bradykinin (−5.4 ± 3.2%), ramiprilat (−4.8 ± 5.0%), and amlodipine (−5.3 ± 5.0%) but had no effect on the tissue response to SNAP (−38 ± 5.8%). Our results indicate that NO can reduce oxygen consumption in the primate myocardium in vitro, and they support a role for the calcium-channel blocker amlodipine as a modulator of myocardial oxygen consumption via a kinin-NO mediated mechanism.

Role of nitric oxide in the coupling of myocardial oxygen consumption and coronary vascular dynamics during pregnancy in the dog

2007 ◽  
Vol 293 (4) ◽  
pp. H2479-H2486 ◽  
Author(s):  
Jeffrey G. Williams ◽  
Tibisay Rincon-Skinner ◽  
Dong Sun ◽  
Zipping Wang ◽  
Suhua Zhang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Oxygen Delivery ◽  
Myocardial Oxygen Consumption ◽  
Left Ventricular ◽  
Tissue Samples ◽  
Enalapril Maleate ◽  
Protein Levels ◽  
Nitrite Production

We examined the ability of cardiac endothelial nitric oxide synthase (eNOS) to couple myocardial oxygen consumption (MV̇o2) and oxygen delivery during pregnancy. Awake dogs were studied using echocardiography before and at 40 days, 50 days, and 60 days (60D) of pregnancy and at ∼14 days postpartum. Left ventricular eNOS, phosphorylated eNOS, and copper, zinc-superoxide dismutase (CuZnSOD or SOD-1) were determined by immunoblotting. MV̇o2 of left ventricular tissue samples was measured in vitro in response to increasing doses of bradykinin, enalapril maleate, and amlodipine. We examined the changes in passive diameter and flow-dependant arteriolar dilation of coronary arterioles. Echocardiography indicated increases in cardiac output (∼60%) during pregnancy. Myocardial eNOS (21 ± 4%), phosphorylated eNOS (19 ± 3%), and SOD-1 (61 ± 2.7%) protein levels were significantly increased at 60D. Bradykinin, enalapril maleate, and amlodipine (10−4 mol/l) decreased MV̇o2 in a nitric oxide-dependant manner (by 24 ± 1.3% in controls and 34 ± 2.2% at 60D; by 21 ± 1.1% in controls and 29 ± 1.1 at 60D; and by 22 ± 2.5% in controls and 26 ± 1.0% at 60D, respectively). Arterioles from pregnant dogs showed increased flow-dependant dilation in response to increased shear stress and larger passive diameter. Nitrite production was stimulated by bradykinin and carbachol in microvessels in vitro; pregnancy enhanced nitrite release. Myocardial eNOS, phosphorylated eNOS, and SOD-1 protein expression are increased during pregnancy, and this increase is associated with enhanced nitric oxide-dependant control of MV̇o2. Thus increases in eNOS and SOD-1 promote the coupling of oxygen delivery and efficiency in the heart during pregnancy.

Blockade of Nitric Oxide Synthesis Reduces Myocardial Oxygen Consumption In Vivo

Circulation ◽  
1997 ◽  
Vol 95 (5) ◽  
pp. 1328-1334 ◽  
Author(s):  
Andrew J. Sherman ◽  
Cornelius A. Davis ◽  
Francis J. Klocke ◽  
Kathleen R. Harris ◽  
Gopalakrishnan Srinivasan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
Nitric Oxide Synthesis

Endogenous nitric oxide modulates myocardial oxygen consumption in canine right ventricle

2001 ◽  
Vol 281 (2) ◽  
pp. H831-H837 ◽  
Author(s):  
Srinath Setty ◽  
Xiaoming Bian ◽  
Johnathan D. Tune ◽  
H. Fred Downey
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Right Ventricular ◽  
Coronary Blood Flow ◽  
Myocardial Oxygen Consumption ◽  
Aortic Pressure ◽  
Coronary Perfusion ◽  
Endogenous Nitric Oxide ◽  
The Right

The role of endogenous nitric oxide (NO) in modulating myocardial oxygen consumption (MV˙o 2) is unclear, in part because of systemic and coronary hemodynamic effects of blocking NO release. This study evaluated the effect of NO on right ventricular MV˙o 2 under controlled hemodynamic conditions. In 12 open-chest dogs, N ω-nitro-l-arginine methyl ester (l-NAME, 150 μg/min), a NO synthase (NOS) blocker, was infused into the right coronary artery. Heart rate and mean aortic pressure were constant. Right coronary blood flow and right ventricular MV˙o 2 were measured at normal and elevated right coronary perfusion pressures (RCP) before and afterl-NAME. To avoid effects of NO synthesis blockade on right coronary blood flow, which might have altered right ventricular MV˙o 2, experiments, were conducted during adenosine-induced maximal coronary vasodilation. l-NAME did not affect right coronary blood flow ( P = 0.51). However,l-NAME significantly increased right ventricular MV˙o 2 (6% at RCP 100 mmHg, and 21% at RCP 180 mmHg). Right coronary blood flow varied with perfusion pressure ( P < 0.02), and the elevation of MV˙o 2 produced by l-NAME increased at higher flows ( P < 0.04), consistent with the greater shear stress-mediated release of NO. These findings indicate that endogenous NO limits right ventricular MV˙o 2.

scholarly journals Nitric Oxide, Myocardial Oxygen Consumption, and ATP Synthesis

1998 ◽  
Vol 83 (10) ◽  
pp. 1067-1068 ◽  
Author(s):  
Joanne S. Ingwall ◽  
Ralph A. Kelly
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
Atp Synthesis

gp91phox-containing NAD(P)H oxidase mediates attenuation of nitric oxide-dependent control of myocardial oxygen consumption by ANG II

2005 ◽  
Vol 289 (2) ◽  
pp. H862-H867 ◽  
Author(s):  
Shintaro Kinugawa ◽  
Juhua Zhang ◽  
Eric Messina ◽  
Erin Walsh ◽  
Harer Huang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
Inflammatory Cells ◽  
Oxygen Electrode ◽  
No Production ◽  
Ang Ii ◽  
Wild Type ◽  
Stimulation Of

We have previously reported that ANG II stimulation increased superoxide anion (O2−) through the activation of NAD(P)H oxidase and inhibited nitric oxide (NO)-dependent control of myocardial oxygen consumption (MV̇o2) by scavenging NO. Our objective was to investigate the role of NAD(P)H oxidase, especially the gp91phox subunit, in the NO-dependent control of MV̇o2. MV̇o2 in mice with defects in the expression of gp91phox [gp91phox(−/−)] was measured with a Clark-type oxygen electrode. Baseline MV̇o2 was not significantly different between wild-type (WT) and gp91phox(−/−) mice. Stimulation of NO production by bradykinin (BK) induced significant decreases in MV̇o2 in WT mice. BK-induced reduction in MV̇o2 was enhanced in gp91phox(−/−) mice. BK-induced reduction in MV̇o2 in WT mice was attenuated by 10−8 mol/l ANG II, which was restored by coincubation with Tiron or apocynin. In contrast to WT mice, BK-induced reduction in MV̇o2 in gp91phox(−/−) mice was not altered by ANG II. There was a decrease in lucigenin (5 × 10−6 mol/l)-detectable O2− in gp91phox(−/−) mice compared with WT mice. ANG II resulted in significant increases in O2− production in WT mice, which was inhibited by coincubation with Tiron or apocynin. However, ANG II had no effect on O2− production in gp91phox(−/−) mice. Histological examination showed that the development of abscesses and/or the invasion of inflammatory cells occurred in lungs and livers but not in hearts and kidneys from gp91phox(−/−) mice. These results indicate that the gp91phox subunit of NAD(P)H oxidase mediates O2− production through the activation of NAD(P)H oxidase and attenuation of NO-dependent control of MV̇o2 by ANG II.

Sign in / Sign up

Export Citation Format

Share Document