Role of abnormal nitric oxide systems in salt-sensitive hypertension.
A large percentage of human hypertensive patients are salt sensitive, referring to the dependence of hypertension on sodium intake, but the cause of the salt sensitivity is not known. Although several mechanisms may contribute to salt-sensitive hypertension, the nitric oxide (NO) system appears to play a major role. Studies in humans and Dahl salt-sensitive (S) rats indicate that NO production is decreased during hypertension. Intravenous L-arginine infusion in Dahl S rats increases NO production and prevents salt-sensitive hypertension. In the Dahl salt-resistant (R) rat, NO production by both inducible NO synthase (iNOS) and neuronal NOS (nNOS) help to prevent salt-sensitive hypertension. Experimental evidence is summarized, indicating that the Dahl S rat has a deficient production of NO by nNOS, although NO production by iNOS appears to moderately decrease salt sensitivity. Other evidence about the importance of NO in salt-sensitive hypertension is reviewed, including the role of the renal NO system.
Manning
R D
RD
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216, USA. dmanning@physiology.umsmed.edu
Hu
L
L
Tan
D Y
DY
Meng
S
S
D000818:Animals; D004305:Dose-Response Relationship, Drug; D006801:Humans; D006973:Hypertension / Q000139:chemically induced* / Q000503:physiopathology*; D007527:Isoenzymes / Q000502:physiology; D007668:Kidney / Q000503:physiopathology; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000502:physiology; D012964:Sodium / Q000008:administration & dosage / Q000494:pharmacology; D012965:Sodium Chloride
D007527:Isoenzymes; D009569:Nitric Oxide; D012965:Sodium Chloride; D012964:Sodium; D019001:Nitric Oxide Synthase