Effects of l-arginine on endothelial and cardiac function in rats with heart failure

Feng, Qingping; Fortin, Amanda J; Lu, Xiangru; Malcolm, Janine; Arnold, Oksana

doi:10.1016/s0014-2999(99)00360-x

Cited by 22 publications

(21 citation statements)

References 31 publications

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“…L-Arginine may have increased NO production by reversing NOS inhibition caused by elevated ADMA or because of its antioxidant properties may have acted directly to reduce O 2 Ϫ levels in contracting muscle. 38 L-Arginine availability may be reduced in heart failure, 39,40 possibly as a result of reduced plasma membrane arginine transport or increased activity of cellular arginases, which metabolize L-arginine as part of the urea cycle. The resultant L-arginine deficiency could contribute to oxidative stress not only by decreasing NO production but also by increasing O 2 Ϫ production by NOS.…”

Section: Discussionmentioning

confidence: 99%

Impaired Modulation of Sympathetic Vasoconstriction in Contracting Skeletal Muscle of Rats With Chronic Myocardial Infarctions

Thomas

Zhang

Victor

2001

Circulation Research

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Abstract-Skeletal muscle perfusion during exercise is impaired in heart failure, but the underlying mechanisms are poorly understood. One possibility is that sympathetic vasoconstriction is enhanced in exercising muscle in heart failure as a result of impaired counterregulatory mechanisms that normally act to attenuate vasoconstrictor responses. In healthy animals, sympathetic vasoconstriction in contracting skeletal muscle is attenuated by endogenously produced nitric oxide (NO). Because the NO pathway may be dysfunctional in heart failure, we hypothesized that reduced NO in contracting muscle would result in enhanced sympathetic vasoconstriction. In sham rats and rats with chronic myocardial infarctions (MIs) produced by coronary artery ligation, we measured arterial pressure and femoral artery blood flow responses to sympathetic nerve stimulation (1, 2.5, and 5 Hz) in resting and contracting hindlimb. In resting hindlimb, sympathetic stimulation decreased femoral vascular conductance similarly in sham and MI rats. In contracting hindlimb, these vasoconstrictor responses were attenuated to a greater extent in sham than in MI rats. NO synthase inhibition enhanced sympathetic vasoconstriction in contracting hindlimb of sham, but not MI, rats. Conversely, infusion of L-arginine or a superoxide scavenger, tempol or tiron, attenuated sympathetic vasoconstriction in contracting hindlimb of MI rats. NO synthase expression was similar, but malondialdehyde (a marker of free radical damage) was greater in skeletal muscle from MI than from sham rats. These data suggest that impaired metabolic modulation of sympathetic vasoconstriction in contracting skeletal muscle of MI rats is a consequence of superoxide-mediated disruption of the NO pathway.

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Section: Discussionmentioning

confidence: 99%

Impaired Modulation of Sympathetic Vasoconstriction in Contracting Skeletal Muscle of Rats With Chronic Myocardial Infarctions

Thomas

Zhang

Victor

2001

Circulation Research

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“…5,11 Mice were anesthetized with sodium pentobarbital (50 mg/kg IP). Atropine (0.05 mg SC) was administered to reduce airway excretion.…”

Section: Induction Of MImentioning

confidence: 99%

“…The infarct size was measured at the end of the experiment and was expressed as a fraction of the total cross-sectional endocardial circumference of the left ventricle (LV). 5,11 …”

Section: Induction Of MImentioning

confidence: 99%

“…5 Briefly, nitrate was converted to nitrite with Aspergillus nitrate reductase, and the total nitrite was measured with the Griess reagent. The absorbance was determined at 540 nm with a spectrophotometer.…”

Section: Nitrate/nitrite Assaymentioning

confidence: 99%

“…4 Recent studies have shown that iNOS expression and activity are increased in the myocardium of failing hearts and result in increased NO levels in the circulation. [5][6][7][8][9] Although increased NO production from iNOS may decrease vascular resistance, which is beneficial, high levels of NO may also depress myocardial contractility and, through formation of peroxynitrite, may cause myocardial damage. 10 In the present study, we hypothesized that increased NO production from iNOS expression causes myocardial dysfunction and results in high mortality after myocardial infarction (MI).…”

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confidence: 99%

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Increased Inducible Nitric Oxide Synthase Expression Contributes to Myocardial Dysfunction and Higher Mortality After Myocardial Infarction in Mice

et al. 2001

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Background-Inducible nitric oxide synthase (iNOS) is expressed in the myocardium after myocardial infarction (MI) and in heart failure. Its pathophysiological role in these conditions, however, is not clear. We hypothesized that increased NO production from iNOS expression causes myocardial dysfunction and results in higher mortality after MI. Methods and Results-MI was induced by left coronary artery ligation in iNOSϪ/Ϫ mutant and wild-type mice. Mortality was followed up for 30 days. MI resulted in a significant increase in mortality in both iNOS Ϫ/Ϫ and wild-type mice compared with sham operation (PϽ0.01). Mortality was significantly decreased and LV myocardial contractility was increased, however, in iNOS Ϫ/Ϫ mice compared with the wild-type mice (PϽ0.05). Five days after MI, myocardial iNOS mRNA expression, plasma nitrate and nitrite concentrations, and myocardial and plasma nitrotyrosine levels were significantly increased in wild-type compared with iNOS Ϫ/Ϫ mutant mice (PϽ0.05). Both basal LV ϩdP/dt and its response to dobutamine were significantly increased in iNOS Ϫ/Ϫ compared with the wild-type mice (PϽ0.05). Conclusions-Increased NO production from iNOS expression contributes to myocardial dysfunction and mortality after MI in mice. (Circulation. 2001;104:700-704.)

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The EFFECTS OF CHRONIC L-Name AND L-Arginine ADMINISTRATION ON Β-Adrenergic RESPONSIVENESS OF STZ-DIABETIC RAT ATRIA

Dinçer

Özçeli̇kay

Demirel-Yılmaz

2000

Pharmacological Research

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Effects of l-arginine on endothelial and cardiac function in rats with heart failure

Cited by 22 publications

References 31 publications

Impaired Modulation of Sympathetic Vasoconstriction in Contracting Skeletal Muscle of Rats With Chronic Myocardial Infarctions

Impaired Modulation of Sympathetic Vasoconstriction in Contracting Skeletal Muscle of Rats With Chronic Myocardial Infarctions

Increased Inducible Nitric Oxide Synthase Expression Contributes to Myocardial Dysfunction and Higher Mortality After Myocardial Infarction in Mice

The EFFECTS OF CHRONIC L-Name AND L-Arginine ADMINISTRATION ON Β-Adrenergic RESPONSIVENESS OF STZ-DIABETIC RAT ATRIA

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