Rapid degradation of prostacyclin (PGI,) inherent to its molecular str
ucture has long been a major limitation in assessing the natriuretic e
ffect of this prostaglandin. The recent availability of the stable PGI
(2) analogue iloprast now allows for a comparative study with prostagl
andin E-2 (PGE(2)). In the present study conducted in six anesthetized
dogs, the intrarenal effects of two consecutive doses (1 and 4 ng.kg(
-1).min(-1)) of PGE(2) on renal blood flow, glomerular filtration rate
, and urinary sodium excretion were compared with the effects of two i
dentical doses of iloprost. The selected doses of PGE(2) were those pr
oducing a maximal natriuretic and vasodilator response without affecti
ng mean arterial pressure. A washout period was allowed between admini
stration of PGE(2) and iloprost. PGE(2) infusion significantly increas
ed fractional sodium excretion from 0.69+/-0.1 to 2.79+/-1.1% and 4.27
+/-1.2%% (P<.05), respectively. These changes in fractional sodium exc
retion induced by PGE(2) were associated with significant increases in
renal blood flow from 151.1+/-62 to 185+/-64.3 and 185.6+/-64.3 mL/mi
n (P<.05), respectively; however: no significant alterations were seen
in glomerular filtration rate: from 29.5+/-9.4 to 35.2+/-12.2 and 32.
7+/-7.8 mL/min (NS)), and mean arterial pressure, from 117.6+/-26 to 1
13.3+/-24.1 and 112.3+/-24.1 mm Hg (NS) during control and PCE2 infusi
on. At identical doses, sequential infusion of PGI(2) had no effect on
renal blood floww and glomerular filtration rate, producing natriures
is only at the highest dose, a fractional sodium excretion from 0.69+/
-0.1 to 0.8+/-0.28 mmHg (NS) and 1.05+/-0.34% (P<.05), respectively. I
n conclusion, the present study confirms that PGE(2) exerts a natriure
tic effect during increases in renal blood flow. In contrast: PGI, had
no hemodynamic effect, and the natriuresis was markedly blunted.