INVESTIGATION OF THE MECHANISM OF SODIUM IiXCPETION IN CONSCICUS RATS : THE ROLE OF THE ENDOGENOUS PROSTAGLANCINS AND THROMBOXANES.
PAPANICOLAOU, N., TSIGGA, M., GKIKA, L-E., HATZIANTONIOU, C., DARLAMETSO-S, I, PARIS, M., FO!IRNIER, A. and BARIETY, J.
Labcratoire de Recherches sur les Hormones du Groupe de Recherches sur la Pathcloqie Renal- et Vasculaire. INSERM U 28, Hbpital Broussais 75014 PARIS France.
The metabolism of sodium was investigated in rats aged 16-17 weeks by means of three studies.
In the first study, we compared the values obtained in 120 normoten- sive wistar rats (60 male and 60 female) (NR), to the values obtained in 88 spontaneously hypertensive Akamoto Aoki rats (40 male and 48 female) (SHR). The SHR group was found to have higher sodium excre- tion rate accompanied by significantly higher renal PGEI, PGE , 6 keto PGF sta ?e chemical metabolite of TXA2) synthesis ; while the creatinine l!
, (the stable chemical metabolite of PG12), PGF2a and TXg2 (the
excretion rate was not found to be significantly different between the two groups.
In the second study, we compared the values obtained in a 100 male rats (60 NR and 40 SHRl (MR) to the values obtained in a 108 female rats (60 NR and 48 SHR) (FR). The FR qrcup was found to have a higher so- dium excretion rate accompanied by a significantly higher renal PGEI, PGE2, 6 keto PGFIa, PGF
$" and TXB2 synthesis ; while the creatinine
excretion rate was foun to be significantly lower.
In the third study, we compared the values obtained in 15 normal rdts before (BACR) and seven days after (ACR) aorta clamping above the renal arteries. The ACR group was found to have significantly lower creati- nine excretion and clearance af creatinine (Ccr) accompanied by signi- ficantly higher renal PGEI, PGE sis and plasma renin activity ( 6
, 6 keto PGFIol, PGF2a and TXB2 synthe- RA) into the renal venous blood ; whi-
le the sodium excretion rate was net found to be significantly diffe- rent.
These results suggest that the increased inhibition of sodium reab- sorption was mediated by the higher renal prostaglandin synthesis. The inhibition was exerted by a direct action and/ or by increasing the non-cortical plasma flow (NCPF). A similar action in the inhibi- tion of sodium reabsorption by TXB2 and renin-angiotensin (R-A) must also be considered.