Kidney prostaglandins

Kidneys Prostaglandins E1( E2, and I2 increase renal blood flow and produce diuresis, natriuresis, and kaliuresis. Prostaglandins E, and E2 antagonize the action of antidiuretic hormones. 

Kidney Prostaglandins (PGE2) normally maintain the blood flow to the kidneys, particularly in the presence of vasoconstrictors. Aspirin reduces prostaglandin levels and increases water and sodium retention. 

Regulation of blood flow and urine processing in the kidney Prostaglandin E (PGE), PGF, PGl (also called prostacyclin), and thromboxanes (TXA)... 

Fauler J, Wiemeyer A, Yoshizawa M, Schurek HJ, Frolich JC Metabolism of cysteinyl leukotrienes by the isolated perfused rat kidney. Prostaglandins 42 239-49,1991... 

Kidneys. Prostaglandins produced in the kidneys cause the renal blood vessels to dilate. The greater flow of blood through the kidney results in increased water and electrolyte excretion. 

Hedqvist, P. (1979). Actions of prostacyclin (PGI ) on adrenergic neuroeffector transmission in the rabbit kidney. Prostaglandins, 17, 249-258... 

Nutmeg extracts have been demonstrated to inhibit the in vitro biosynthesis of prostaglandin by rat kidney tissue, and ground nutmeg fed orally to rats has decreased kidney prostaglandin levels, these effects being similar to those produced by indomethacin. ... 

Aminophenol is a selective nephrotoxic agent and intermpts proximal tubular function (121,122). Disagreement exists concerning the nephrotoxity of the other isomers although they are not as potent as 4-aminophenol (123,124). Respiration, oxidative phosphorylation, and ATPase activity are inhibited in rat kidney mitochondria (125). The aminophenols and their derivatives are inhibitors of 5-Hpoxygenase (126) and prostaglandin synthetase... 

In addition to being involved in the formation of urine, the kidney acts as an endocrine organ secreting renin, erythropoietin, prostaglandins (qv), and kinins it is also capable of synthesizing substances such as la,25-dihydroxycholecalciferol [32222-06-3] One of the principal functions of the... 

Cyclooxygenase (COX) activity is responsible for the formation of prostaglandins from their arachidonic acid precursor. Two COX isoforms have been identified, COX-1 and COX-2. While COX-1 is constitutively expressed in most tissues, COX-2 is typically only found after induction by proinflammatory stimuli. However, a constitutively expressed and highly regulated COX-2 is found in the kidney, both in the renal medulla and in the renal cortex. Renal cortical COX-2 is located in the area ofthe juxtaglomerular apparatus, and prostaglandins formed by COX-2 regulate the expression and secretion of renin in response to a reduction in NaCl concentration at the macula densa. 

Endothelial cells are the major source of ET-1-synthesis. ET-1 is also produced by astrocytes, neurons, hepatocytes, bronchial epithelial cells, renal epithelial and mesangial cells. Physiological stimuli of ET-1-synthesis in endothelial cells are angiotensin II, catecholamines, thrombin, growth factors, insulin, hypoxia and shear stress. Inhibitors of ET-1 synthesis are atrial natriuretic peptide, prostaglandin E2 and prostacyclin. ET-2 is mainly synthesized in kidney, intestine, myocardium and placenta and ET-3 is predominantely produced by neurons, astrocytes and renal epithelial cells. 

Cooper, C.L. and Malik, K.U. (1985). Prostaglandin synthesis and renal vasoconstriction elicited by adrenergic stimuli are linked to activation of alpha-1 adrenergic receptors in the isolated rat kidney. J. Pharmacol. Exp. Ther. 233, 24-31. 

Schlondorff, D. and Ardaillon, R. (1986). Prostaglandins and other arachidonic acid metabolites in the kidney. Kidney Int. 29, 108-119. 

Li+ also inhibits several hormone-stimulated adenylate cyclases which, in some cases, appear to be related to side effects of Li+ therapy. For instance, Li+ inhibits the hydro-osmotic action of vasopressin, the antidiuretic hormone which increases water resorption in the kidney [136]. This effect is associated with polyuria, a relatively harmless side effect sometimes experienced with Li+ treatment, which arises from the inability of the kidney to concentrate urine. Li+ has been shown to inhibit vasopressin-stimulated adenylate cyclase activity in renal epithelial cells. Additionally, Li+ is reported to enhance the vasopressin-induced synthesis of prostaglandin E2 (PGE2) in vitro in kidney. PGE2 inhibits adenylate cyclase activity by stimulation of Gj, and, therefore, this effect may contribute to the Li+-induced polyuria. 

Anamura S, Dohi T, Shirakawa M, et al. 1988. Effects of phenolic dental medicaments on prostaglandin synthesis by microsomes of bovine tooth pulp and rabbit kidney medulla. Arch Oral Biol 33 355-360. 

In addition to their involvement in excretion and metabolism, the kidneys also have endocrine functions. They produce the hormones erythropoietin and calcitriol and play a decisive part in producing the hormone angiotensin II by releasing the enzyme renin. Renal prostaglandins (see p. 390) have a local effect on Na resorption. 

III.a.4.3. Changes in renal blood flow. Blood flow through the kidney is partially controlled by the production of renal vasodilatory prostaglandins. If the synthesis of these prostaglandins is inhibited (e.g. by indomethacin), the renal excretion of lithium is reduced with a subsequent rise in serum levels. The mechanism underlying this interaction is not entirely clear, as serum lithium levels are unaffected by some potent prostaglandin synthetase inhibitors (e.g. aspirin). If an NSAID is prescribed for a patient taking lithium the serum levels should be closely monitored. 

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