Prostaglandins and the kidney

Abstract

This review provides a summary and assessment of research involving renal prostaglandins. Arachidonic acid released from phospholipids is converted by prostaglandin cycle-oxygenase in the kidney to PGE2, PGF2α, PGD2, and, possibly, to PGI2, and thromboxane A2. Production of PGE2, and PGF2α, is predominately but not exclusively in the medulla, whereas degradative enzymes are present in both cortex and medulla. Prostaglandins enter the tubular lumen by facilitated transport and are partially reabsorbed from the urine in the distal nephron. Urine prostaglandins probably reflect renal synthesis. PGE2 and endoperoxides stimulate and PGF2α and indomethacin inhibit renal renin synthesis. In response to ischemia, vasoconstriction, or angiotensin II the kidney increases prostaglandin synthesis to modulate renal vascular resistance. In conscious animals or man no role has been established for prostaglandins in the maintenance of basal renal blood flow or renal sodium excretion. PGE influences renal water excretion by inhibiting the action vasopressin. Despite conflicting data there is evidence that renal prostaglandins are involved either primarily or secondarily in many types of hypertension. Inhibitors of prostaglandin cyclooxygenase have been used with success in Bartter's syndrome. Conflicting results in many areas of investigation may be resolved by the use of more accurate and reliable assays, careful handling of samples, and the use of urine to further investigate renal prostaglandin synthesis. prostaglandin synthesis; renin-angiotensin; hypertension; antidiuretic hormone

Correction of proximal tubule phosphate transport defect inHypmicein vivoandin vitrowith indomethacin

“…PGs oppose vasoconstrictor hormones that reduce the glomerular filtration rate (36,37,(41)(42)(43). Thus, indomethacin could potentially reduce phosphate excretion by reducing the filtered load of phosphate delivered to the proximal tubule.…”

Diclofenac toxicity in Gyps vulture is associated with decreased uric acid excretion and not renal portal vasoconstriction

“…Furthermore with valve control being mediated by the beta adrenergic and muscarinic receptors (Burrows et al, 1983), and not the prostaglandins, Meteyer hypothesis appears to be inaccurate. The theory does, however, have merit in that renal vascular tone is maintained by PG making it plausible that DF could influence the PGs mediating venodialation thereby induce ischemia (Dunn and Hood, 1977).…”

Effect of tienoxolol, a new diuretic β‐blocking agent, on urinary prostaglandin excretion in the rat

“…Prostacyclin (PGI2) mainly produced in the glomerulus, modulates cortical functions (maintenance or increase of renal blood flow, regulation of glomerular filtration rate, renin secretion) (Anderson et al, 1976;Weber et al, 1976;Dunn & Hood, 1977;Whorton et al, 1977;Terragno et al, 1978). Prostaglandin E2 (PGE2), synthesized primarily in the papilla, regulates medullary functions (water, sodium and chloride excretion) (Anderson et al, 1976;Fine & Trizna, 1977;Stokes, 1979;Sraer et al, 1982).…”