Investigation on the mechanism of prostaglandins release

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.…”

Prostaglandins in rat tissues

“…The phenomenon was almost imperceptible when the animals were binephrectomized (Papanicolaou, 1972). In experiments in which blood was cross-circulated in rats the blood pressure of the recipient dropped while that of the donor rose following the increase of circulating blood volume produced by infusion of either saline or blood.…”

Relationship between Glomerular Filtration Rate and Tubular Reabsorption of Sodium in Patients with Unilateral Renal Artery Stenosis.

“…The absence of correlation shown in figure 3 does not really exclude such an hypothesis. Several factors, including in hibition of cortical extraction and intrarenal blood flow redistribution could influence the Epahchanges in humans [15][16][17][18],soexplaining the lack of relationship in individual changes in net tubular reabsorption of sodium did not correlate with the respective changes in Epah ( fig.3), it is not possible to suggest a causal relationship between the decrease in sodium reabsorption and the decrease in Epah-Intrarenal infusion of prostaglandins has been shown to produce natriuresis and de creased Epah [19][20][21][22], In addition, saline in fusion in normotensive and hypertensive sub jects and/or in animals has been found to be associated with decreased Epah and increased release of prostaglandins by the kidney [23][24][25]. On the other hand, there is evidence that prostaglandins inhibit uptake of PAH by kid ney cortical slices in vitro [26].…”