L-arginine in the prevention and treatment of cardiovascular disease: From basic to clinical research studies

PierMarco Piatti, Emanuela Setola, Pietro Lucotti, Elena Galluccio, Lucilla D. Monti

Research output: Contribution to journalArticle

Abstract

L-arginine is a basic endogenous amino acid and is a precursor of nitric oxide (NO). NO is synthesized from L-arginine by a family of enzymes, called NO synthases (NOS). The constitutively expressed NOS isoforms, endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS), are likely to be the major contributors to whole-body NO production. NO is an important signalling molecule in the cardiovascular system regulating vascular tone, platelet activity, monocyte adhesion, thrombosis and is intimately involved in the development of atherosclerosis. Impaired NO mediated-endothelial function has been observed in patients with established coronary, peripheral arterial disease and in patients with metabolic syndrome and type 2 diabetes. Several experimental and clinical studies showed a beneficial effect of L-arginine on endothelium in conditions associated with impaired NO bioavailability. In vitro studies have shown that L-arginine induced NO-mediated-vasodilation and a complex antiaggregatory, anticoagulatory, profibrinolytic and antiatherogenic activity. In humans, L-arginine therapy can augment vascular dilation and inhibit platelet aggregation under certain conditions. Long term administration of L-arginine was able to ameliorate peripheral insulin sensitivity through a normalization of NO/cGMP pathway in type 2 diabetic patients while acute infusion of L-arginine significantly increased forearm blood and decreased endothelin-1 levels in subjects with microvascular angina through increased nitric oxide bioavailability. The mechanism of action of L-arginine may involve NOS provision, mainly in patients with elevated levels of the endogenous NOS inhibitor asymmetric dimethylarginine. Therefore, a novel therapeutic role of L-arginine in the prevention and treatment of endothelial dysfunction and cardiovascular disease should be considered.

Original languageEnglish
Pages (from-to)185-191
Number of pages7
JournalVascular Disease Prevention
Volume3
Issue number3
DOIs
Publication statusPublished - 2006

Fingerprint

Arginine
Nitric Oxide
Cardiovascular Diseases
Research
Nitric Oxide Synthase
Therapeutics
Biological Availability
Blood Vessels
Microvascular Angina
Clinical Studies
Basic Amino Acids
Nitric Oxide Synthase Type I
Nitric Oxide Synthase Type III
Peripheral Arterial Disease
Endothelin-1
Cardiovascular System
Platelet Aggregation
Forearm
Vasodilation
Type 2 Diabetes Mellitus

Keywords

  • Cardiovascular disease
  • Endothelium
  • Insulin resistance
  • L-arginine
  • Prevention
  • Type 2 diabetes

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Epidemiology

Cite this

L-arginine in the prevention and treatment of cardiovascular disease : From basic to clinical research studies. / Piatti, PierMarco; Setola, Emanuela; Lucotti, Pietro; Galluccio, Elena; Monti, Lucilla D.

In: Vascular Disease Prevention, Vol. 3, No. 3, 2006, p. 185-191.

Research output: Contribution to journalArticle

@article{dc459d0f4412448599b63bc4ec549925,
title = "L-arginine in the prevention and treatment of cardiovascular disease: From basic to clinical research studies",
abstract = "L-arginine is a basic endogenous amino acid and is a precursor of nitric oxide (NO). NO is synthesized from L-arginine by a family of enzymes, called NO synthases (NOS). The constitutively expressed NOS isoforms, endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS), are likely to be the major contributors to whole-body NO production. NO is an important signalling molecule in the cardiovascular system regulating vascular tone, platelet activity, monocyte adhesion, thrombosis and is intimately involved in the development of atherosclerosis. Impaired NO mediated-endothelial function has been observed in patients with established coronary, peripheral arterial disease and in patients with metabolic syndrome and type 2 diabetes. Several experimental and clinical studies showed a beneficial effect of L-arginine on endothelium in conditions associated with impaired NO bioavailability. In vitro studies have shown that L-arginine induced NO-mediated-vasodilation and a complex antiaggregatory, anticoagulatory, profibrinolytic and antiatherogenic activity. In humans, L-arginine therapy can augment vascular dilation and inhibit platelet aggregation under certain conditions. Long term administration of L-arginine was able to ameliorate peripheral insulin sensitivity through a normalization of NO/cGMP pathway in type 2 diabetic patients while acute infusion of L-arginine significantly increased forearm blood and decreased endothelin-1 levels in subjects with microvascular angina through increased nitric oxide bioavailability. The mechanism of action of L-arginine may involve NOS provision, mainly in patients with elevated levels of the endogenous NOS inhibitor asymmetric dimethylarginine. Therefore, a novel therapeutic role of L-arginine in the prevention and treatment of endothelial dysfunction and cardiovascular disease should be considered.",
keywords = "Cardiovascular disease, Endothelium, Insulin resistance, L-arginine, Prevention, Type 2 diabetes",
author = "PierMarco Piatti and Emanuela Setola and Pietro Lucotti and Elena Galluccio and Monti, {Lucilla D.}",
year = "2006",
doi = "10.2174/156727006778019068",
language = "English",
volume = "3",
pages = "185--191",
journal = "Vascular Disease Prevention",
issn = "1567-2700",
publisher = "Bentham Science Publishers B.V.",
number = "3",

}

TY - JOUR

T1 - L-arginine in the prevention and treatment of cardiovascular disease

T2 - From basic to clinical research studies

AU - Piatti, PierMarco

AU - Setola, Emanuela

AU - Lucotti, Pietro

AU - Galluccio, Elena

AU - Monti, Lucilla D.

PY - 2006

Y1 - 2006

N2 - L-arginine is a basic endogenous amino acid and is a precursor of nitric oxide (NO). NO is synthesized from L-arginine by a family of enzymes, called NO synthases (NOS). The constitutively expressed NOS isoforms, endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS), are likely to be the major contributors to whole-body NO production. NO is an important signalling molecule in the cardiovascular system regulating vascular tone, platelet activity, monocyte adhesion, thrombosis and is intimately involved in the development of atherosclerosis. Impaired NO mediated-endothelial function has been observed in patients with established coronary, peripheral arterial disease and in patients with metabolic syndrome and type 2 diabetes. Several experimental and clinical studies showed a beneficial effect of L-arginine on endothelium in conditions associated with impaired NO bioavailability. In vitro studies have shown that L-arginine induced NO-mediated-vasodilation and a complex antiaggregatory, anticoagulatory, profibrinolytic and antiatherogenic activity. In humans, L-arginine therapy can augment vascular dilation and inhibit platelet aggregation under certain conditions. Long term administration of L-arginine was able to ameliorate peripheral insulin sensitivity through a normalization of NO/cGMP pathway in type 2 diabetic patients while acute infusion of L-arginine significantly increased forearm blood and decreased endothelin-1 levels in subjects with microvascular angina through increased nitric oxide bioavailability. The mechanism of action of L-arginine may involve NOS provision, mainly in patients with elevated levels of the endogenous NOS inhibitor asymmetric dimethylarginine. Therefore, a novel therapeutic role of L-arginine in the prevention and treatment of endothelial dysfunction and cardiovascular disease should be considered.

AB - L-arginine is a basic endogenous amino acid and is a precursor of nitric oxide (NO). NO is synthesized from L-arginine by a family of enzymes, called NO synthases (NOS). The constitutively expressed NOS isoforms, endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS), are likely to be the major contributors to whole-body NO production. NO is an important signalling molecule in the cardiovascular system regulating vascular tone, platelet activity, monocyte adhesion, thrombosis and is intimately involved in the development of atherosclerosis. Impaired NO mediated-endothelial function has been observed in patients with established coronary, peripheral arterial disease and in patients with metabolic syndrome and type 2 diabetes. Several experimental and clinical studies showed a beneficial effect of L-arginine on endothelium in conditions associated with impaired NO bioavailability. In vitro studies have shown that L-arginine induced NO-mediated-vasodilation and a complex antiaggregatory, anticoagulatory, profibrinolytic and antiatherogenic activity. In humans, L-arginine therapy can augment vascular dilation and inhibit platelet aggregation under certain conditions. Long term administration of L-arginine was able to ameliorate peripheral insulin sensitivity through a normalization of NO/cGMP pathway in type 2 diabetic patients while acute infusion of L-arginine significantly increased forearm blood and decreased endothelin-1 levels in subjects with microvascular angina through increased nitric oxide bioavailability. The mechanism of action of L-arginine may involve NOS provision, mainly in patients with elevated levels of the endogenous NOS inhibitor asymmetric dimethylarginine. Therefore, a novel therapeutic role of L-arginine in the prevention and treatment of endothelial dysfunction and cardiovascular disease should be considered.

KW - Cardiovascular disease

KW - Endothelium

KW - Insulin resistance

KW - L-arginine

KW - Prevention

KW - Type 2 diabetes

UR - http://www.scopus.com/inward/record.url?scp=33746870836&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33746870836&partnerID=8YFLogxK

U2 - 10.2174/156727006778019068

DO - 10.2174/156727006778019068

M3 - Article

AN - SCOPUS:33746870836

VL - 3

SP - 185

EP - 191

JO - Vascular Disease Prevention

JF - Vascular Disease Prevention

SN - 1567-2700

IS - 3

ER -