Hypertension, Vol 7, 357-363, Copyright © 1985 by American Heart Association
JP Koepke and GF DiBona
The effects of high sodium intake (drinking 0.9% NaCl for 15 days) on the
increased renal sympathetic nerve activity and decreased urinary sodium
excretion resulting from stressful environmental stimulation (air jet to
head) were examined in conscious spontaneously hypertensive rats (SHR) and
normotensive Wistar-Kyoto rats (WKY). On a normal sodium intake in SHR, air
stress increased renal sympathetic nerve activity 77% and decreased urinary
sodium excretion 28% without altering effective renal plasma flow or
glomerular filtration rate. By contrast, in conscious SHR on high sodium
intake, the same air stress caused a greater increase in renal sympathetic
nerve activity (103%) and a greater antinatriuresis (42%) along with
reductions in effective renal plasma flow and glomerular filtration rate.
Surgical renal denervation prevented the antinatriuretic responses to air
stress in other conscious SHR on high or normal sodium intake. In conscious
WKY, air stress had no effect on renal sympathetic nerve activity or
urinary sodium excretion, regardless of normal or high sodium intake. We
conclude that the enhanced renal sympathetic nerve activity and
antinatriuretic responses to air stress in conscious SHR on high sodium
intake are dependent on a centrally mediated facilitation of sympathetic
neural outflow to the kidney. The greater antinatriuretic response to air
stress in conscious SHR than in WKY may reflect a greater genetic
predisposition in SHR to increase renal sympathetic nerve activity during
air stress.
ARTICLES
High sodium intake enhances renal nerve and antinatriuretic responses to stress in spontaneously hypertensive rats
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