Ms. Mozaffari et al., RENAL RESPONSES TO HYPERTONIC SALINE INFUSION IN SALT-SENSITIVE SPONTANEOUSLY HYPERTENSIVE RATS, The American journal of the medical sciences, 314(6), 1997, pp. 370-376
In Wistar Kyoto (WKY) and Sprague Dawley rats, high dietary sodium chl
oride (NaCl) increases natriuretic and diuretic responses to acute iso
tonic saline infusion, but in NaCl-sensitive spontaneously hypertensiv
e rats (SHR-S), a high-NaCl diet causes negligible increases in natriu
retic and diuretic responses. To investigate whether this deficit in s
odium and fluid excretion in SHR-S is stimulus (volume)-specific or be
cause of a more generalized alteration in renal function, the present
study measured, in SHR-S and Wistar Kyoto rats, natriuretic and diuret
ic responses to a hypertonic saline infusion (the amount of sodium inf
used was equal to that infused in a previous, isotonic experiment). Ei
ght-week-old Wistar Kyoto rats, SHR-S, and salt-resistant SHR were giv
en a basal (1%) or high (8%)-NaCl diet for 2 weeks. Intravenous infusi
on of hypertonic saline increased mean arterial pressure and reduced h
eart rate in all groups. Baseline sodium excretion was lower in SBR-S
compared with salt-resistant SHR with either diet, but; after infusion
of hypertonic saline, all 6 groups displayed significant increases in
sodium and fluid excretion, glomerular filtration rate, and effective
renal blood flow (ERBF). The percent-sodium excretion in response to
hypertonic saline infusion was slightly, but significantly, lower in S
HR-S (compared with salt-resistant SHR) for either the basal or the hi
gh-NaCl diet, We conclude that renal responses to hypertonic saline in
fusion are affected minimally in SI-IR-S compared with sale-resistant
SHR or Wistar Kyoto rats. Therefore, the deficits in renal function ob
served in SHR-S after volume loading are not reflected in a renal defi
cit to hypertonic saline challenge.