Salt sensitivity in genetically hypertensive rats of the Lyon strain

Citation
M. Florin et al., Salt sensitivity in genetically hypertensive rats of the Lyon strain, KIDNEY INT, 59(5), 2001, pp. 1865-1872
Citations number
39
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
KIDNEY INTERNATIONAL
ISSN journal
00852538 → ACNP
Volume
59
Issue
5
Year of publication
2001
Pages
1865 - 1872
Database
ISI
SICI code
0085-2538(200105)59:5<1865:SSIGHR>2.0.ZU;2-S
Abstract
Background. 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 pres ent work was aimed to determine whether LH rats were salt sensitive in chro nic conditions. In addition, a protocol was developed to determine the rena l function curve in freely moving rats. Methods. Fourteen-week-old rats either untreated or orally treated since we aning with perindopril (3 mg/kg/24 h), an angiotensin-converting enzyme inh ibitor, or with valsartan (15 mg/kg/24 h), an angiotensin II subtype 1 rece ptor antagonist, so as to eliminate the influence of endogenous changes in angiotensin formation were used. Blood pressure (BP) and urinary sodium exc retion were measured before, during an oral salt load (2% NaCl in drinking water), and during a two-week aldosterone infusion (50 mug/kg/24 h subcutan enusly). Results. NaCl induced a greater BP increase in untreated LH rats than in LN and IL controls. Perindopril normalized the BP of LH rats but not its elev ation during a salt load. Aldosterone slightly increased BP in LH and LL ra ts 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 chron ic renal function curve in freely moving rats. Conclusion. The present work demonstrates that LH rats are salt sensitive. This characteristic manifests despite the lack of an active renin-angiotens in system and is not explained by a hypersensitivity to aldosterone.