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Promising New Drug Targets for Refractory Hypertension

Gail D. Thomas, PhD; Weiguo Zhang, MD, PhD; Ronald G. Victor, MD

JAMA. 2001;285:2055-2057.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

The nitric oxide pathway contributes to the blood pressure–lowering effects of many commonly used therapeutic agents and emerging basic research on this pathway is elucidating potential new antihypertensive drug targets. Understanding the regulation of the nitric oxide pathway also provides a conceptual framework for understanding the potential role played by nitric oxide in a number of disorders, including congestive heart failure, atherosclerosis, nitrate tolerance, muscular dystrophy, circulatory shock, and male sexual dysfunction.

Nitric Oxide Pathway

Nitric oxide is produced by the enzyme nitric oxide synthase (NOS) during the oxidation of the amino acid substrate L-arginine to L-citrulline.¹ Three distinct NOS isoforms are found in mammalian cells: endothelial NOS (eNOS or NOS III), neuronal NOS (nNOS or NOS I), and inducible NOS (iNOS or NOS II). Under normal physiological conditions, iNOS is undetectable in macrophages and other tissues, and thus appears to . . . [Full Text of this Article]

Decreased NOS Expression as a Cause of Hypertension

Endogenous NOS Inhibitors as a Cause of Hypertension

Superoxide Production as a Cause of Nitric Oxide-Deficient Hypertension

Perspective

Author Affiliations: Department of Internal Medicine, Hypertension Division, and the Donald W. Reynolds Cardiovascular Clinical Research Center, University of Texas Southwestern Medical Center, Dallas.

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