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,1, and
1 Department of Physiology,
Sodium ions absorbed from the intestine are
postulated to act on the liver to reflexly suppress renal sympathetic
nerve activity (RSNA), resulting in inhibition of sodium reabsorption
in the kidney. To test the hypothesis that the renal sympathoinhibitory response to portal venous NaCl infusion involves an action of arginine
vasopressin (AVP) at the area postrema, we examined the effects of
portal venous infusion of hypertonic NaCl on RSNA before and after
lesioning of the area postrema (APL) or after pretreatment with an AVP
V1 receptor antagonist (AVPX).
Rabbits were chronically instrumented with portal and femoral venous
catheters, femoral arterial catheters, and renal nerve electrodes.
Portal venous infusion of 9.0% NaCl (0.02, 0.05, 0.10, and 0.15 ml · kg
1 · min
1
of 9.0% NaCl for 10 min) produced a dose-dependent suppression of RSNA
(
12 ± 3,
34 ± 3,
62 ± 5, and 80 ± 2%, respectively) that was greater than that produced by femoral vein
infusion of 9.0% NaCl (2 ± 3,
3 ± 2,
12 ± 4, and
33 ± 3%, respectively). The suppression of RSNA
produced by portal vein infusion of 9.0% NaCl was partially reversed
by pretreatment with AVPX (
9 ± 3,
20 ± 3,
41 ± 4, and
55 ± 4%, respectively) and by APL
(
11 ± 2,
25 ± 2,
49 ± 3, and
59 ± 6%, respectively). There were no significant differences between
the effects of AVPX and APL, and the effect of APL was not augmented by
AVPX. These results indicate that the suppression of RSNA due to portal
venous infusion of 9.0% NaCl involves an action of AVP via the area
postrema.
sodium chloride; hepatorenal reflex; vasopressin; neurohumoral interaction; area postrema
Deceased 19 February 1996.
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