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
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
KIDNEY INTERNATIONAL
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.