Renal Prostaglandins and Other Eicosanoids

Abstract

The sections in this article are: Biochemistry Eicosanoid Synthesis Eicosanoid Degradation Lipoxygenase and Epoxygenase Derivatives of Arachidonic Acid Sites of Renal Eicosanoid Synthesis Mechanism of Peptide Hormone Stimulation of Eicosanoid Synthesis Eicosanoid Receptors and Mechanism of Action of Eicosanoids Prostaglandin Excretion and Secretion Influence of Prostaglandins on Renal Blood Flow and Glomerular Filtration Rate Administration of Prostaglandins and Their Precursors Influence of Cyclooxygenase Inhibition on Renal Blood Flow and Glomerular Filtration Role of Prostaglandins in Renal Autoregulation and Tubuloglomerular Feedback Hormonal Stimulation of Renal Prostaglandin Synthesis Peptide Hormones and Prostaglandin Interactions in the Control of Renal Blood Flow Some Conditions in Which Prostaglandins Exert an Important Vasodilatory Action Summary: Prostaglandins and Renal Hemodynamics Prostaglandins and Renal Water Excretion Capacity of Renal Prostaglandins to Modulate Water Excretion in the Presence of Vasopressin Capacity of Renal Prostaglandins to Modulate Water Excretion When Vasopressin Is Absent or Severely Reduced Vasopressin and Vasopressin Analogs Stimulate Prostaglandin Synthesis in the Kidney Mechanisms by Which Prostaglandins Modulate Renal Water Excretion Prostaglandin Antagonism of AVP ‐Stimulated Water Flow: A Physiologic Phenomenon Mediated through the cyclic‐ AMP System? Summary: Prostaglandins and Renal Water Excretion Staglandins and Sodium Excretion Influence of Prostaglandins and Arachidonic Acid on Renal Sodium Excretion Cyclooxygenase Inhibition and Renal Sodium Excretion Effect of Sodium Intake on Renal Prostaglandin Synthesis and Excretion Nephron Sites Where Prostaglandins Oppose Sodium Absorption Summary: Prostaglandins and Sodium Excretion Contribution of Prostaglandins to the Renal Release of Renin Effects of Exogenous Prostaglandins and Arachidonic Acid on Renal Renin Release Influence of Cyclooxygenase Inhibition on Renal Renin Release Renin Release by the β‐Adrenergic, Renal Baroreceptor, and Macula Densa Mechanisms: Role of Prostaglandins Summary: Prostaglandins and Renin Release Prostaglandins as Mediators of Erythropoietin Release Effect of Prostaglandins on Tubular Transport of Calcium, Phosphate, and Magnesium, and on Renal Ammoniagenesis Calcium Phosphate Magnesium Renal Ammoniagenesis

Renal Medullary Infusion of Indomethacin and Adenosine

“…Most of the reported data indicated that renal PG, especially PGE2, are natriuretic, depending on their inhibitory action on NaCl transport in the ascending limb of Henle's loop and medullary collecting duct; they can also inhibit transport and increase renal excretion indirectly, secondary to intrarenal vasodilatation [11,12,20]. However, when PG were not given systemically but directly into renal tissue, using porous matrix cylinders placed in the cortico-medullary border area, antinatriuresis and an inhibition of proximal reabsorption were reported, apparently mediated by increased generation of angiotensin II and consequent stimulation of the proximal transport [21,22].…”

“…However, when PG were not given systemically but directly into renal tissue, using porous matrix cylinders placed in the cortico-medullary border area, antinatriuresis and an inhibition of proximal reabsorption were reported, apparently mediated by increased generation of angiotensin II and consequent stimulation of the proximal transport [21,22]. Elimination of endogenous PG by administration of inhibitors, such as indomethacin, has usually led to moderate antidiuresis, whereas the effect on U Na V was not uniform: a decrease or no change were most often reported [11]. As an exception, in two early studies natriuresis was reported in conscious dogs [23] and in humans [24].…”

“…Here attention was focused on postulated effects of adenosine on tubular transport of water and urine concentration [10]. Both prostaglandins and adenosine were reported to induce different renal effects, depending on the route of administration [11][12][13].…”

Reactive oxygen species and molecular regulation of renal oxygenation

“…Since the 1950s, many autocrines or paracrines have been reported to participate in the renal medullary adaptation to low P O 2 such as prostaglandin E 2 (PG E 2 ), adenosine (Ado), and nitric oxide (NO) (Brezis et al. 1991, Conrad & Dunn 1992, Roman & Zou 1993, Zou & Cowley 1997, Zou et al. 1999).…”

“…As have demonstrated in other organs or tissues, the renal medulla has naturally developed various adaptive mechanisms to protect the cells from ischaemic and hypoxic injury in face of low P O 2 (Brezis et al. 1991, 1994, Conrad & Dunn 1992, Epstein 1997). Recently, there is accumulating evidence indicating that hypoxia‐induced molecular adaptation in mammalian tissues or cells is associated with the molecular regulation of gene expression and functional activity of oxygen‐sensitive gene products and this molecular adaptation is importantly attributed to local redox status.…”