Nitric Oxide Spares Myocardial Oxygen Consumption Through Attenuation of Contractile Response to β-Adrenergic Stimulation in Patients With Idiopathic Dilated Cardiomyopathy

Circulation ◽  
2000 ◽  
Vol 101 (16) ◽  
pp. 1925-1930 ◽  
Author(s):  
Toshiro Shinke ◽  
Hideyuki Takaoka ◽  
Motoshi Takeuchi ◽  
Katsuya Hata ◽  
Hiroya Kawai ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Dilated Cardiomyopathy ◽  
Myocardial Oxygen Consumption ◽  
Contractile Response ◽  
Idiopathic Dilated Cardiomyopathy ◽  
Adrenergic Stimulation

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.

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