Effect of systemic nitric oxide synthase inhibition on arterial stiffness in humans

Jun Sugawara; Hidehiko Komine; Koichiro Hayashi; Mutsuko Yoshizawa; Takashi Yokoi; Takeshi Otsuki; Nobutake Shimojo; Takashi Miyauchi; Seiji Maeda; Hirofumi Tanaka

doi:10.1291/hypres.30.411

Effect of systemic nitric oxide synthase inhibition on arterial stiffness in humans

Jun Sugawara^*, Hidehiko Komine, Koichiro Hayashi, Mutsuko Yoshizawa, Takashi Yokoi, Takeshi Otsuki, Nobutake Shimojo, Takashi Miyauchi, Seiji Maeda, Hirofumi Tanaka

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

45 Citations (Scopus)

Abstract

Stiffening of large elastic arteries impairs the buffering function of the arterial system and contributes to cardiovascular disease. The aim of this study was to determine whether endothelium-derived nitric oxide (NO) modulates the stiffness of large elastic arteries in humans. Seven apparently healthy adults (60±3 years, 2 males and 5 females) underwent systemic α-adrenergic blockade (phentolamine) and systemic NO synthase inhibition using N^G-monomethyl-L-arginine (L-NMMA) in sequence. Phentolamine was given first to isolate contribution of NO to arterial stiffness by preventing reflex changes in sympathetic tone that result from systemic NO synthase inhibition, and also to compare arterial stiffness at a similar mean arterial pressure. Mean arterial blood pressure decreased (p<0.05) after phentolamine infusion but returned to baseline levels after L-NMMA infusion. The carotid β-stiffness index (via simultaneous ultrasound and applanation tonometry on the common carotid artery) did not change after the restraint of systemic α-adrenergic nerve activity (9.8±1.2 vs. 9.1±1.1 U) but increased (p<0.05) after NO synthase inhibition (12.6±2.0 U). These results suggest that NO appears to modulate central arterial stiffness in humans.

Original language	English
Pages (from-to)	411-415
Number of pages	5
Journal	Hypertension Research
Volume	30
Issue number	5
DOIs	https://doi.org/10.1291/hypres.30.411
Publication status	Published - 2007 May
Externally published	Yes

Keywords

Arterial compliance
Endothelium
Sympathetic nervous system

ASJC Scopus subject areas

Internal Medicine
Physiology
Cardiology and Cardiovascular Medicine

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1291/hypres.30.411

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abstract = "Stiffening of large elastic arteries impairs the buffering function of the arterial system and contributes to cardiovascular disease. The aim of this study was to determine whether endothelium-derived nitric oxide (NO) modulates the stiffness of large elastic arteries in humans. Seven apparently healthy adults (60±3 years, 2 males and 5 females) underwent systemic α-adrenergic blockade (phentolamine) and systemic NO synthase inhibition using NG-monomethyl-L-arginine (L-NMMA) in sequence. Phentolamine was given first to isolate contribution of NO to arterial stiffness by preventing reflex changes in sympathetic tone that result from systemic NO synthase inhibition, and also to compare arterial stiffness at a similar mean arterial pressure. Mean arterial blood pressure decreased (p<0.05) after phentolamine infusion but returned to baseline levels after L-NMMA infusion. The carotid β-stiffness index (via simultaneous ultrasound and applanation tonometry on the common carotid artery) did not change after the restraint of systemic α-adrenergic nerve activity (9.8±1.2 vs. 9.1±1.1 U) but increased (p<0.05) after NO synthase inhibition (12.6±2.0 U). These results suggest that NO appears to modulate central arterial stiffness in humans.",

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AU - Otsuki, Takeshi

AU - Shimojo, Nobutake

AU - Miyauchi, Takashi

AU - Maeda, Seiji

AU - Tanaka, Hirofumi

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AB - Stiffening of large elastic arteries impairs the buffering function of the arterial system and contributes to cardiovascular disease. The aim of this study was to determine whether endothelium-derived nitric oxide (NO) modulates the stiffness of large elastic arteries in humans. Seven apparently healthy adults (60±3 years, 2 males and 5 females) underwent systemic α-adrenergic blockade (phentolamine) and systemic NO synthase inhibition using NG-monomethyl-L-arginine (L-NMMA) in sequence. Phentolamine was given first to isolate contribution of NO to arterial stiffness by preventing reflex changes in sympathetic tone that result from systemic NO synthase inhibition, and also to compare arterial stiffness at a similar mean arterial pressure. Mean arterial blood pressure decreased (p<0.05) after phentolamine infusion but returned to baseline levels after L-NMMA infusion. The carotid β-stiffness index (via simultaneous ultrasound and applanation tonometry on the common carotid artery) did not change after the restraint of systemic α-adrenergic nerve activity (9.8±1.2 vs. 9.1±1.1 U) but increased (p<0.05) after NO synthase inhibition (12.6±2.0 U). These results suggest that NO appears to modulate central arterial stiffness in humans.

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Effect of systemic nitric oxide synthase inhibition on arterial stiffness in humans

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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