Effect of l-arginine on acetylcholine-induced endothelium-dependent vasodilation differs between the coronary and forearm vasculatures in humans

Yoshitaka Hirooka, Kensuke Egashira, Tsutomu Imaizumi, Tatsuya Tagawa, Hisashi Kai, Masaru Sugimachi, Akira Takeshita

Research output: Contribution to journalArticle

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Abstract

Objectives. The goal of this study was to determine whether the elect of l-arginine on endothelium-dependent vasoditation evoked with acetylcholine differs between the coronary and forearm vasculatures in humans. Background. Administration of l-arginine, a substrate in the production of endothetium-derived nitric oxide, may stimulate the release of nitric oxide. Methods. Seven patients with normal coronary angiograms and seven with mild coronary artery disease and hypertension underwent coronary arteriography and an intracoronary Doppler catheter technique, and the diameter of the large epicardial coronary artery and coronary blood flow were measured. Forearm blood flow was measured by use of a strain gauge plethysmograph. Results. Before l-arginine administration, acetylcholine (1 to 30 μg/min) increased coronary blood flow with modest vasoconstriction of a large coronary artery. Acetylcholine (4 to 24 μg/min) also increased forearm blood flow. The acetylcholine-induced increases in coronary and forearm blood flow were significantly less in patients with coronary artery disease than in control patients. Intracoronary infusion of l-arginine at 50 mg/min did not alter responses of the large coronary artery diameter or coronary blood flow to acetyicholine in either group. In contrast, l-arginine at 10 mg/min significantly (p < 0.01) augmented the forearm blood flow response to acetylcholine (4 to 24 μg/min) to a similar extent in the two groups. Conclusions. The effect of l-arginine on acetylcholine-induced vasodilation difers between the coronary and forearm vasculatures in humans. It is suggested that impaired acetylcholine-induced coronary and forearm vasodilation in patients with coronary artery disease and hypertension may not be related to a limited availability of l-arginine.

Original languageEnglish
Pages (from-to)948-955
Number of pages8
JournalJournal of the American College of Cardiology
Volume24
Issue number4
DOIs
Publication statusPublished - Oct 1994

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Forearm
Vasodilation
Acetylcholine
Endothelium
Arginine
Coronary Artery Disease
Coronary Vessels
Angiography
Nitric Oxide
Hypertension
Vasoconstriction
Catheters

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

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Effect of l-arginine on acetylcholine-induced endothelium-dependent vasodilation differs between the coronary and forearm vasculatures in humans. / Hirooka, Yoshitaka; Egashira, Kensuke; Imaizumi, Tsutomu; Tagawa, Tatsuya; Kai, Hisashi; Sugimachi, Masaru; Takeshita, Akira.

In: Journal of the American College of Cardiology, Vol. 24, No. 4, 10.1994, p. 948-955.

Research output: Contribution to journalArticle

Hirooka, Yoshitaka ; Egashira, Kensuke ; Imaizumi, Tsutomu ; Tagawa, Tatsuya ; Kai, Hisashi ; Sugimachi, Masaru ; Takeshita, Akira. / Effect of l-arginine on acetylcholine-induced endothelium-dependent vasodilation differs between the coronary and forearm vasculatures in humans. In: Journal of the American College of Cardiology. 1994 ; Vol. 24, No. 4. pp. 948-955.
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abstract = "Objectives. The goal of this study was to determine whether the elect of l-arginine on endothelium-dependent vasoditation evoked with acetylcholine differs between the coronary and forearm vasculatures in humans. Background. Administration of l-arginine, a substrate in the production of endothetium-derived nitric oxide, may stimulate the release of nitric oxide. Methods. Seven patients with normal coronary angiograms and seven with mild coronary artery disease and hypertension underwent coronary arteriography and an intracoronary Doppler catheter technique, and the diameter of the large epicardial coronary artery and coronary blood flow were measured. Forearm blood flow was measured by use of a strain gauge plethysmograph. Results. Before l-arginine administration, acetylcholine (1 to 30 μg/min) increased coronary blood flow with modest vasoconstriction of a large coronary artery. Acetylcholine (4 to 24 μg/min) also increased forearm blood flow. The acetylcholine-induced increases in coronary and forearm blood flow were significantly less in patients with coronary artery disease than in control patients. Intracoronary infusion of l-arginine at 50 mg/min did not alter responses of the large coronary artery diameter or coronary blood flow to acetyicholine in either group. In contrast, l-arginine at 10 mg/min significantly (p < 0.01) augmented the forearm blood flow response to acetylcholine (4 to 24 μg/min) to a similar extent in the two groups. Conclusions. The effect of l-arginine on acetylcholine-induced vasodilation difers between the coronary and forearm vasculatures in humans. It is suggested that impaired acetylcholine-induced coronary and forearm vasodilation in patients with coronary artery disease and hypertension may not be related to a limited availability of l-arginine.",
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T1 - Effect of l-arginine on acetylcholine-induced endothelium-dependent vasodilation differs between the coronary and forearm vasculatures in humans

AU - Hirooka, Yoshitaka

AU - Egashira, Kensuke

AU - Imaizumi, Tsutomu

AU - Tagawa, Tatsuya

AU - Kai, Hisashi

AU - Sugimachi, Masaru

AU - Takeshita, Akira

PY - 1994/10

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N2 - Objectives. The goal of this study was to determine whether the elect of l-arginine on endothelium-dependent vasoditation evoked with acetylcholine differs between the coronary and forearm vasculatures in humans. Background. Administration of l-arginine, a substrate in the production of endothetium-derived nitric oxide, may stimulate the release of nitric oxide. Methods. Seven patients with normal coronary angiograms and seven with mild coronary artery disease and hypertension underwent coronary arteriography and an intracoronary Doppler catheter technique, and the diameter of the large epicardial coronary artery and coronary blood flow were measured. Forearm blood flow was measured by use of a strain gauge plethysmograph. Results. Before l-arginine administration, acetylcholine (1 to 30 μg/min) increased coronary blood flow with modest vasoconstriction of a large coronary artery. Acetylcholine (4 to 24 μg/min) also increased forearm blood flow. The acetylcholine-induced increases in coronary and forearm blood flow were significantly less in patients with coronary artery disease than in control patients. Intracoronary infusion of l-arginine at 50 mg/min did not alter responses of the large coronary artery diameter or coronary blood flow to acetyicholine in either group. In contrast, l-arginine at 10 mg/min significantly (p < 0.01) augmented the forearm blood flow response to acetylcholine (4 to 24 μg/min) to a similar extent in the two groups. Conclusions. The effect of l-arginine on acetylcholine-induced vasodilation difers between the coronary and forearm vasculatures in humans. It is suggested that impaired acetylcholine-induced coronary and forearm vasodilation in patients with coronary artery disease and hypertension may not be related to a limited availability of l-arginine.

AB - Objectives. The goal of this study was to determine whether the elect of l-arginine on endothelium-dependent vasoditation evoked with acetylcholine differs between the coronary and forearm vasculatures in humans. Background. Administration of l-arginine, a substrate in the production of endothetium-derived nitric oxide, may stimulate the release of nitric oxide. Methods. Seven patients with normal coronary angiograms and seven with mild coronary artery disease and hypertension underwent coronary arteriography and an intracoronary Doppler catheter technique, and the diameter of the large epicardial coronary artery and coronary blood flow were measured. Forearm blood flow was measured by use of a strain gauge plethysmograph. Results. Before l-arginine administration, acetylcholine (1 to 30 μg/min) increased coronary blood flow with modest vasoconstriction of a large coronary artery. Acetylcholine (4 to 24 μg/min) also increased forearm blood flow. The acetylcholine-induced increases in coronary and forearm blood flow were significantly less in patients with coronary artery disease than in control patients. Intracoronary infusion of l-arginine at 50 mg/min did not alter responses of the large coronary artery diameter or coronary blood flow to acetyicholine in either group. In contrast, l-arginine at 10 mg/min significantly (p < 0.01) augmented the forearm blood flow response to acetylcholine (4 to 24 μg/min) to a similar extent in the two groups. Conclusions. The effect of l-arginine on acetylcholine-induced vasodilation difers between the coronary and forearm vasculatures in humans. It is suggested that impaired acetylcholine-induced coronary and forearm vasodilation in patients with coronary artery disease and hypertension may not be related to a limited availability of l-arginine.

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