What is the clinical evidence from this study?

Study design: Other. Population: Healthy adults (n=7). Intervention: L-NMMA (Nitric Oxide Synthase Inhibitor) vs. Phentolamine (α-adrenergic blockade). Primary outcome: Carotid β-stiffness index (p=<0.05).

January 1, 2007Open Access

Effect of Systemic Nitric Oxide Synthase Inhibition on Arterial Stiffness in Humans

Q: What are the key findings of this study?

Systemic nitric oxide synthase inhibition with L-NMMA significantly increased the carotid β-stiffness index from 9.1 to 12.6 U (p<0.05), indicating that nitric oxide modulates central arterial stiffness.

JSJun SugawaraTokyo University of Foreign Studies HKHidehiko KomineNational Institute of Advanced Industrial Science and Technology KHKoichiro HayashiKanazawa University

Key Result

Systemic nitric oxide synthase inhibition with L-NMMA significantly increased the carotid β-stiffness index from 9.1 to 12.6 U (p<0.05), indicating that nitric oxide modulates central arterial stiffness.

Structured PICO

Does systemic NO synthase inhibition increase arterial stiffness in healthy adults?

Population

7 healthy, sedentary older adults (mean age 60 years, 71% female) underwent sequential systemic α-adrenergic blockade and NO synthase inhibition to assess arterial stiffness.

Intervention

Systemic NO synthase inhibition using NG-monomethyl-L-arginine (L-NMMA) administered after systemic alpha-adrenergic blockade (phentolamine)

Comparator

Baseline after systemic alpha-adrenergic blockade (phentolamine) alone

Outcome

Carotid beta-stiffness index (measured via simultaneous ultrasound and applanation tonometry on the common carotid artery)surrogate

Systemic nitric oxide synthase inhibition increases central arterial stiffness in humans, demonstrating that endothelium-derived nitric oxide modulates large elastic artery stiffness.

Main Result

Absolute Event Rate: 12.6% vs 9.1%

p-value: p=<0.05

Limitations

Small number of subjects, which may lack statistical power to detect some changes.
Use of older subjects whose NO bioavailability may already be declined, potentially underestimating NO's contribution to arterial stiffness.

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 alpha-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 beta-stiffness index (via simultaneous ultrasound and applanation tonometry on the common carotid artery) did not change after the restraint of systemic alpha-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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