Mt. Llinas et al., INTERACTIONS BETWEEN ANGIOTENSIN AND NITRIC-OXIDE IN THE RENAL RESPONSE TO VOLUME EXPANSION, American journal of physiology. Regulatory, integrative and comparative physiology, 38(3), 1995, pp. 504-510
This study examined, in anesthetized dogs, the possible interactions b
etween nitric oxide (NO) and angiotensin II (ANG II) in mediating the
renal response to an extracellular volume expansion (ECVE). It was fou
nd that the intrarenal maintenance of ANG II levels (group 1) or the i
ntrarenal 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 th
ird 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 synthes
is inhibition is mediated by endogenous ANG II levels. In the fourth g
roup, it was observed that NO synthesis inhibition, during the intrare
nal maintenance of ANG II levels, induced a decrease of renal blood fl
ow (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 t
his group suggest that endogenous NO modulates the vasoconstrictor and
antinatriuretic effects of ANG II during an ECVE. In summary, the res
ults of this study suggest that there is an important interaction betw
een NO and ANG II in mediating the renal response to an ECVE.