Jy. Mu et al., THE INTESTINAL-TRACT AND THE PATHOPHYSIOLOGY OF ARTERIAL-HYPERTENSION- AN EXPERIMENTAL-STUDY ON DAHL RATS, Acta Physiologica Scandinavica, 155(2), 1995, pp. 137-146
Salt depleted rabbits and humans excrete an oral sodium load more quic
kly via the kidneys than an intravenous one. This has been ascribed to
the presence of a sodium sensor in the gastrointestinal tract which i
n some way can influence renal function. The purpose of this study was
to investigate this response in the Dahl rats. Renal and faecal sodiu
m excretion was followed in the two strains of rats (normotensive, sal
tresistant (SR/Jr) and hypertensive, saltsensitive (SS/Jr) rats). Afte
r 4 days on a low salt diet they were given NaCl (1.5 mmol kg(-1) body
wt) either by gavage or intravenously. SR/Jr rats showed an increased
renal sodium excretion both after oral and intravenous sodium repleti
on. The excretion was 2-3 times greater after the oral than after the
intravenous administration. The SS/Jr rats augmented their renal sodiu
m excretion only after the oral load, although the sodium excretion wa
s significantly less than in SR/Jr rats. In fact, during the first 8 h
after giving sodium orally the renal excretion of sodium was on an av
erage eight times larger in the SR/Jr than in the SS/Jr rats. Renal ex
cretion of sodium was similar in the two strains after intravenous adm
inistration. We conclude that the hypertensive SS/Jr rats have great d
ifficulties in excreting an oral sodium load, a phenomenon that may be
of importance in the pathophysiology of arterial hypertension in this
strain of rats.