Interactions between angiotensin and nitric oxide in the renal
response to volume expansion.
Llin[acute]as, Maria T., Juan D. Gonz[acute]alez, F. Javier Salazar.
Departamento de Fisiolog[acute]ia, Facultad de Medicina, Murcia,
SPAIN.
APStracts 2:0057R, 1995.
The purpose of this study was to examine, in anesthetized dogs, the
possible interactions between nitric oxide (NO) and angiotensin II
(Ang II) in mediating the renal response to an extracellular volume
expansion (ECVE). It was found that the intrarenal maintenance of Ang
II levels (group 1), or the intrarenal NO synthesis inhibition (group
2), did not induce changes in renal hemodynamics but reduced (p<0.05)
the ECVE-induced increments in sodium excretion and fractional
lithium excretion (FeLi). In the third group, Ang II synthesis was
inhibited during NO synthesis blockade. It was found in this group
that the NO synthesis inhibition reduced the ECVE-induced increment
in sodium excretion (p<0.05) but did not modify the ECVE-induced
increment in FeLi. These results suggest that the increase of
proximal sodium reabsorption induced by the NO synthesis inhibition
is mediated by endogenous Ang II levels. In the fourth group, it was
observed that NO synthesis inhibition, during the intrarenal
maintenance of Ang II levels, induced a decrease of renal blood flow
(p<0.05) and reduced the natriuretic response to ECVE to a lower
level (p<0.05) than that observed in groups 1 and 2. The results of
this group suggest that endogenous NO modulates the vasoconstrictor
and antinatriuretic effects of Ang II during an ECVE. In summary the
results of this study suggest that there is an important interaction
between NO and Ang II in mediating the renal response to an ECVE.
Received 26 September 1994; accepted in final form 14 February
1995.
APS Manuscript Number R555-4.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 7 March 1995.