Tags

Type your tag names separated by a space and hit enter

Interaction between nitric oxide and angiotensin II in the endothelium: role in atherosclerosis and hypertension.
J Hypertens Suppl 2006; 24(1):S45-50JH

Abstract

BACKGROUND

Although there is overwhelming evidence that hypertension promotes atherosclerosis, the relative contribution and/or interaction of vasoactive and hemodynamic factors remain undefined. Endothelial dysfunction complicates hypertension and is a precursor of atherosclerosis. It is characterized by a reduction in the bioavailability of vasodilators, particularly nitric oxide, and an increase in the activity of vasoconstrictors, including angiotensin (Ang) II and reactive oxygen species (ROS). Nitric oxide antagonizes the vasoconstrictive and pro-atherosclerotic effects of Ang II, whereas Ang II decreases nitric oxide bioavailability by promoting oxidative stress.

OBJECTIVES

The present review will focus on the interaction among nitric oxide, Ang II, and ROS in the endothelium and will examine their role in vascular tone and atherogenesis. In this context, studies from our laboratory will be reviewed demonstrating that salt-sensitive hypertension is a vascular diathesis characterized by a local activation of Ang II and NAD(P)H oxidase-derived ROS in the setting of insufficient nitric oxide. In hypertensive Dahl salt-sensitive rats, a paradigm of human salt-sensitive hypertension, inhibition of Ang II type 1 receptor or NAD(P)H oxidase-derived ROS prevented the development of endothelial dysfunction, upregulation of pro-atherogenic molecules, and vascular ROS generation, independently of blood pressure.

CONCLUSIONS

Salt sensitivity, an independent risk factor for increased cardiovascular morbidity and mortality, affects approximately 50% of hypertensives. Our studies suggest that, in salt-sensitive hypertension, atherogenesis is more closely linked to oxidative stress than to the hemodynamic stress of hypertension. To prevent or arrest atherosclerosis, antihypertensive therapy should aim at restoring the homeostatic balance between vasoactive factors in the vascular wall.

Authors+Show Affiliations

Nephrology and Hypertension Section, Veterans Affairs Medical Center and Division of Nephrology and Hypertension and Vascular Biology Institute, University of Miami Miller School of Medicine, Miami, Florida 33125, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, Non-P.H.S.
Review

Language

eng

PubMed ID

16601573

Citation

Schulman, Ivonne Hernandez, et al. "Interaction Between Nitric Oxide and Angiotensin II in the Endothelium: Role in Atherosclerosis and Hypertension." Journal of Hypertension. Supplement : Official Journal of the International Society of Hypertension, vol. 24, no. 1, 2006, pp. S45-50.
Schulman IH, Zhou MS, Raij L. Interaction between nitric oxide and angiotensin II in the endothelium: role in atherosclerosis and hypertension. J Hypertens Suppl. 2006;24(1):S45-50.
Schulman, I. H., Zhou, M. S., & Raij, L. (2006). Interaction between nitric oxide and angiotensin II in the endothelium: role in atherosclerosis and hypertension. Journal of Hypertension. Supplement : Official Journal of the International Society of Hypertension, 24(1), pp. S45-50.
Schulman IH, Zhou MS, Raij L. Interaction Between Nitric Oxide and Angiotensin II in the Endothelium: Role in Atherosclerosis and Hypertension. J Hypertens Suppl. 2006;24(1):S45-50. PubMed PMID: 16601573.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interaction between nitric oxide and angiotensin II in the endothelium: role in atherosclerosis and hypertension. AU - Schulman,Ivonne Hernandez, AU - Zhou,Ming-Sheng, AU - Raij,Leopoldo, PY - 2006/4/8/pubmed PY - 2006/7/6/medline PY - 2006/4/8/entrez SP - S45 EP - 50 JF - Journal of hypertension. Supplement : official journal of the International Society of Hypertension JO - J Hypertens Suppl VL - 24 IS - 1 N2 - BACKGROUND: Although there is overwhelming evidence that hypertension promotes atherosclerosis, the relative contribution and/or interaction of vasoactive and hemodynamic factors remain undefined. Endothelial dysfunction complicates hypertension and is a precursor of atherosclerosis. It is characterized by a reduction in the bioavailability of vasodilators, particularly nitric oxide, and an increase in the activity of vasoconstrictors, including angiotensin (Ang) II and reactive oxygen species (ROS). Nitric oxide antagonizes the vasoconstrictive and pro-atherosclerotic effects of Ang II, whereas Ang II decreases nitric oxide bioavailability by promoting oxidative stress. OBJECTIVES: The present review will focus on the interaction among nitric oxide, Ang II, and ROS in the endothelium and will examine their role in vascular tone and atherogenesis. In this context, studies from our laboratory will be reviewed demonstrating that salt-sensitive hypertension is a vascular diathesis characterized by a local activation of Ang II and NAD(P)H oxidase-derived ROS in the setting of insufficient nitric oxide. In hypertensive Dahl salt-sensitive rats, a paradigm of human salt-sensitive hypertension, inhibition of Ang II type 1 receptor or NAD(P)H oxidase-derived ROS prevented the development of endothelial dysfunction, upregulation of pro-atherogenic molecules, and vascular ROS generation, independently of blood pressure. CONCLUSIONS: Salt sensitivity, an independent risk factor for increased cardiovascular morbidity and mortality, affects approximately 50% of hypertensives. Our studies suggest that, in salt-sensitive hypertension, atherogenesis is more closely linked to oxidative stress than to the hemodynamic stress of hypertension. To prevent or arrest atherosclerosis, antihypertensive therapy should aim at restoring the homeostatic balance between vasoactive factors in the vascular wall. SN - 0952-1178 UR - https://www.unboundmedicine.com/medline/citation/16601573/Interaction_between_nitric_oxide_and_angiotensin_II_in_the_endothelium:_role_in_atherosclerosis_and_hypertension_ L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=linkout&SEARCH=16601573.ui DB - PRIME DP - Unbound Medicine ER -