Pyrogenic Renal Hyperemia: The Role of Prostaglandins

Abstract

The intravenous administration of triple typhoid vaccine to anesthetized dogs resulted in a significant increase in renal blood flow accompanied by a modest decline in systemic blood pressure. This renal hyperemia was associated with elevated renal secretory rates of renin and prostaglandin E and F. Measurements of the intracortical distribution of radiolabeled microspheres revealed a progressive decrease in outer cortical blood flow rates and a progressive increase in inner cortical flow rates. When meclofenamate, an inhibitor of prostaglandin synthetase, was administered concomitantly with triple typhoid vaccine renal hyperemia did not develop. The renal renin secretory rate increased modestly and intracortical renal blood flow was not redistributed. The increased renal blood flow after triple typhoid vaccine administration to unanesthetized dogs was also reversed by meclofenamate. The marked increase in prostaglandin secretion by the kidney during renal hyperemia following triple typhoid vaccine administration (pyrogen), and the effect of meclofenamate, is consonant with a role for increased renal synthesis and release of prostaglandins.

Isolated Hypoaldosteronism and Abnormalities in Renin, Kallikrein, and Prostaglandin

“…Urine and serum creatinine were measured using a Beckman creatinine ana lyzer model 2 (Beckman Instruments, Brea, Calif., USA). Cortisol, PRA, PGE2, and aldosterone were determined by radioimmunoas say [17][18][19] and urinary kallikrein by a radiochemical method [20], Samples for PRA were collected in prechilled glass tubes containing 10.5 mg disodium EDTA and immediately centrifuged at 0°C, the plasma separated and placed in polystyrene tubes for storage at -20 °C prior to assay. To assay for PRA, 10 ul of maleate buffer was added to 1 ml of the sample.…”

The importance of anti‐lipid A (anti‐endotoxin): Prevention of “shock lung” and acute renal failure

“…However, if the patient receives adequate fluid replacement, as in postoperative care, often there is only a polyuric renal failure [22]. This corresponds to a phase of hyperemia of the inner renal cortex and medulla that is due to increased synthesis and release of E-prostaglandins, which is provoked by low-grade endotoxinemia [23]. Commonly, acute oliguric renal failure does develop because the lipid-A of endotoxins causes sympathetic nervous vasoconstriction; release of catecholamines that reinforces that vasoconstriction; activation of the renin-angiotensin mechanism; and disseminated or local intrarenal coagulation (DIC).…”