Effects of Saline Infusion on Prostaglandin-like Materials in Renal Venous Blood and Medulla of Canine Kidney

Abstract

SUMMARYAn activity of prostaglandin (PG)-like substances was measured in venous blood and renal medullary tissue of dogs. The PG-like substances were extracted by silica gel column chromatography and their activity was measured by rat vasodepressor bioassay. The activity of PGE-like substance both in renal venous blood and medulla was greater in saline infused dogs than in control, non-infused dogs. The possibility was discussed that the increased activity of PGE in kidney may be involved in the mechanisms of natriuresis in saline-loaded animals. Additional Indexing Words: Blood volume expansion Natriuretic factors NatriuresisT has been demonstrated that prostaglandin E and A increase renal blood flow, urine flow and sodium excretion.1),2) Prostaglandin E (PGE) has also been shown to inhibit the effect of vasopressin in vitro3) and possibly in vivo.4) Natural occurrence of prostaglandins in renal tissue5),6) together with their effects on kidney functions suggested that prostaglandins may play a physiological role in the regulation of sodium and water excretion.The present experiments were designed to examine the effects of saline infusion on prostaglandins concentration in the renal venous blood and renal medullary tissue. METHODCollection of blood and renal tissue: Female mongrel dogs weighing 7-12Kg, fasted and thirsted overnight prior to the experiments, were anesthetized with sodium pentobarbital (25mg/Kg, iv). The left kidney was exposed retroperitoneally by the flank incision and the left ureter was catheterized. After the infusion of 0.9% NaCl (150ml/Kg) into the cubital vein for 120 or 150min, the needle connected with plastic tube was inserted into the left renal vein and about 200ml of blood was withdrawn into a syringe containing

The Effect of Indomethacin and Prostaglandin (PGE2) on Renal Failure Due to Glycerol in Saline-Loaded Rats

“…We have further shown that the addition of PGE2, which reduces peripheral resistance and increases renal plasma flow and glomerular filtration rate as well as sodium and water excretion (Johnston et al, 1967;Vander, 1968;Shimizu et al, 1969;Hornych et al, 1973), to the saline infusion restored protection by saline even after the administration of indomethacin Because prostaglandins are released by saline infusion (Papanicolaou, 1972;Shimizu et al, 1973) we have concluded that in this model of experimental acute renal failure the partial protection afforded by saline infusion may result from the renal stimulatory effect on prostaglandin synthesis and the inhibition of renin synthesis and release (Gross & Vander, 1968;Gavras et al, 1970).…”

“…It is established that infusion of 150 mmol/I sodium chloride (saline) protects against acute renal failure caused by glycerol (Wilson, Thiel, Arce & Oken, 1967 Since saline infusion has been shown to induce the release of prostaglandins (Papanicolaou, 1972;Shimizu, Yamamoto & Yoshitoshi, 1973), which are known to increase renal blood flow (Johnston, Herzog & Lauler, 1967;Vander, 1968;Shimizu, Kurosawa, Maeda & Yoshitoshi, 1969;Hornych, Safar, Papanicolaou, Meyer & Milliez, 1973) and to inhibit the renal effects of pressor systems (McGiff, Terragno, Crowshaw & Lonigro, 1970), we decided to investigate whether the protective effect of saline infusion against acute renal failure could be attributed to release of prostaglandins.…”

The Release of Renal Prostaglandins during Saline Infusion in Normal and Hypertensive Subjects

“…It was suggested that a considerable proportion of the prostaglandin-like substance released was of renal origin (Papanicolaou, 1972), and this has subsequently been confirmed in dogs (Shimizu, Yamamoto & Yoshitoshi, 1973).…”

Prostaglandins and the kidney

“…The first approach has not yielded consistent data, possibly because of severe limitations with most of the prostaglandin assays employed in these studies. PGE, and, occasionally PGF or PGA, were measured in renal venous blood (178,197,215), renal tissue (14, 220), urine (230), and peripheral plasma (246) in man (178,246), rabbits (14, 230), dogs (197,215), and rats (220). These authors reported that sodium loading or volume expansion increased renal venous PGE (178,197,215), reduced renal tissue (220) and urinary PGE (230), and decreased PGA in peripheral plasma (246) and in renal papilla (but not cortex or medulla) (14).…”

“…We believe, however, that a significant portion of the TABLE 2. Assays for prostaglandins and thromboxanes 1) Bioassay a) Superfused organs (rat stomach, rat colon, and chick rectum) (61, 142) b) Single organ (rabbit aorta, gerbil colon) (151, 220) c) Cell assay (platelet aggregation) (151) d) Bat vasodepressor response in vivo (161,197) 2) Badioimmunoassay a) "Specific" antibodies to PGE, PGF, TXB2, etc. (49,83,84,181,202) b) Convert PGE to PGB and use PGB antisera (56,81,243) 3) Bat liver radioreceptor assay for PGE (71) 4) Gas chromatography-mass spectroscopy (71,192) 3.…”