INTERACTIONS BETWEEN ANGIOTENSIN AND NITRIC-OXIDE IN THE RENAL RESPONSE TO VOLUME EXPANSION

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.