Salt sensitivity in genetically hypertensive rats of the Lyon strain

Abstract

Genetically hypertensive (LH) rats of the Lyon strain exhibit a blunted pressure-natriuresis function when compared, in acute conditions, with their normotensive (LN) and low blood pressure (LL) controls. The present work was aimed to determine whether LH rats were salt sensitive in chronic conditions. In addition, a protocol was developed to determine the renal function curve in freely moving rats. Fourteen-week-old rats either untreated or orally treated since weaning with perindopril (3 mg/kg/24 h), an angiotensin-converting enzyme inhibitor, or with valsartan (15 mg/kg/24 h), an angiotensin II subtype 1 receptor antagonist, so as to eliminate the influence of endogenous changes in angiotensin formation were used. Blood pressure (BP) and urinary sodium excretion were measured before, during an oral salt load (2% NaCl in drinking water), and during a two-week aldosterone infusion (50 microg/kg/24 h subcutaneously). NaCl induced a greater BP increase in untreated LH rats than in LN and LL controls. Perindopril normalized the BP of LH rats but not its elevation during a salt load. Aldosterone slightly increased BP in LH and LL rats either untreated or treated with valsartan. Finally, the combination of telemetric BP measurement with 24-hour urine collection when salt was added to drinking water allowed accurate determination of the slope of the chronic renal function curve in freely moving rats. The present work demonstrates that LH rats are salt sensitive. This characteristic manifests despite the lack of an active renin-angiotensin system and is not explained by a hypersensitivity to aldosterone.