Brain angiotensinergic pathways mediate renal nerve inhibition by
central hypertonic saline in conscious sheep.
May, C. N., and R. M. McAllen.
Howard Florey Institute of Physiology and Medicine, University of
Melbourne, Parkville 3052, Australia
APStracts 3:0348R, 1996.
The renal sympathetic responses to infusion of hypertonic solutions
into the lateral cerebral ventricles were investigated in conscious
sheep. Intracerebroventricular (ICV) infusion of artificial
cerebrospinal fluid (CSF) containing 0.6M NaCl, at 1mL/h for 20 min,
reduced renal sympathetic nerve activity (RSNA) by 81 +/- 5% (n=6,
P<0.001). Plasma renin concentration also fell (P<0.05),
while arterial pressure increased by 6.4 +/- 0.7 mmHg (P<0.01).
ICV hypertonic sorbitol (0.9M in CSF at 1mL/h) had no effect. The AT
-1 receptor antagonist losartan (1mg/h) abolished the plasma renin and
arterial pressure responses to ICV hypertonic saline, and
significantly reduced the fall in RSNA to 17 +/- 10% (P<0.001).
During ICV hypertonic saline the baroreflex relation of RSNA to
diastolic pressure was shifted to the left, and that to central
venous pressure was abolished, when compared to control relations
obtained by manipulating pressure with intravenous phenylephrine.
These findings indicate that: (i) RSNA is inhibited by a central
mechanism that senses high sodium (or perhaps chloride) concentration
rather than hypertonicity; (ii) this inhibition occurs independently
of reflexes from high and low pressure baroreceptors, although these
may enhance the inhibition, (iii) inhibition of RSNA by hypertonic
saline involves a central angiotensinergic pathway.
Received 10 April 1996; accepted in final form 30 August 1996.
APS Manuscript Number R206-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996