Salt-sensitive hypertension: lessons from animal models.
The underlying etiology of salt-sensitive hypertension has been elusive, in part because the term represents a syndrome rather than a specific disease entity and in part because of the difficulty in completely defining the characteristics of the syndrome. The introduction of inbred models of salt-sensitive hypertension has facilitated understanding blood pressure response to dietary salt. Careful examination of one of these models, the Dahl/Rapp rat, has shown that the L-arginine:nitric acid (NO) pathway is integrally involved in production of hypertension in response to an increase in dietary salt. This review provides an overview of NO, salt sensitivity, and the role of NO in the pathogenesis of salt-sensitive hypertension.
Sanders
P W
PW
Nephrology Research and Training Center, Department of Medicine, University of Alabama at Birmingham and Veterans Affairs Medical Center, 35294-0007, USA.
D000818:Animals; D001120:Arginine / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D004195:Disease Models, Animal; D006801:Humans; D006973:Hypertension / Q000209:etiology*; D009569:Nitric Oxide / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D017207:Rats, Sprague-Dawley; D017673:Sodium Chloride, Dietary / Q000009:adverse effects*
D017673:Sodium Chloride, Dietary; D009569:Nitric Oxide; D001120:Arginine