Jm. Pinilla et al., ROLE OF PROSTAGLANDINS ON THE RENAL EFFECTS OF ANGIOTENSIN AND INTERSTITIAL PRESSURE DURING VOLUME EXPANSION, The American journal of physiology, 265(6), 1993, pp. 180001469-180001474
This study was undertaken to determine, in anesthetized dogs, the role
of renal prostaglandins (PG) in mediating the natriuretic response to
increased renal interstitial hydrostatic pressure (RIHP) during extra
cellular volume expansion (ECVE) with isotonic Wine. It was also deter
mined if the intrarenal angiotensin Il (ANG II) effects during ECVE ar
e potentiated by the inhibition of PG synthesis. ECVE induced similar
elevations of RIHP, natriuresis, and fractional lithium excretion in d
ogs treated (n = 7) and not treated with a PG synthesis inhibitor (n =
5). In other experimental groups, the effects of the intrarenal maint
enance of ANG II levels (n = 6) by infusing captopril and ANG II into
the right renal artery were compared with those induced by the simulta
neous infusion of captopril, ANG II, and a PG synthesis inhibitor (n =
6). In response to ECVE, renal blood flow and glomerular filtration r
ate were similar in both kidneys when ANG II levels were maintained co
nstant and were significantly higher in the left kidney when ANG II le
vels were maintained constant and PG synthesis was inhibited in the ri
ght kidney. However, when compared with the left kidney, the ECVE-indu
ced increments of natriuresis and RIHP in the right kidney were reduce
d by the same magnitude when intrarenal ANG II was maintained constant
with (36 and 53%, respectively) and without (40 and 54%, respectively
) the simultaneous PG synthesis inhibition. Our results indicate that
during ECVE, renal PGs do not play an important role in mediating the
RIHP-induced increments in natriuresis and decrements in proximal sodi
um reabsorption. Furthermore, it is suggested that PG synthesis inhibi
tion does not potentiate the antinatriuretic effects of ANG II during
ECVE.