Kidney prostaglandins actions

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. 

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

Another area of prostaglandin action which has been studied in detail is their role in water-retention by the kidney. The final event in urine production occurs in the terminal portion of the renal tubule where ADH... 

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. 

Loop diuretics induce renal prostaglandin synthesis, and these prostaglandins participate in the renal actions of these drugs. NSAIDs (eg, indomethacin) can interfere with the actions of the loop diuretics by reducing prostaglandin synthesis in the kidney. This interference is minimal in otherwise normal subjects but may be significant in patients with nephrotic syndrome or hepatic cirrhosis. 

Purdy KE, Arendshorst WJ EP(1) and EP(4) receptors mediate prostaglandin E(2) actions in the microcirculation of rat kidney. Am.J.Physiol Renal Physiol 279 F755-F764, 2000... 

Many drugs and other chemicals can adversely affect renal function by directly or indirectly affecting the reabsorption of electrolytes and water in the kidney. Chlorpropamide can enhance the secretion of ADH and promote the water conservation actions of the hormone, while lithium use can lead to a nephrogenic diabetes insipidus. NSAIDs block the formation of renal prostaglandins, which can result in hyperkalemia. Hyperkalemia may also result from the use of beta blockers, potassium-sparing diuretics, and cyclosporine. 

The endocrine functions of the kidneys may be regarded either as primary, because the kidneys are endocrine organs producing hormones, or as secondary, because the kidneys are a site of action for hormones produced or activated elsewhere. In addition, the kidneys are a site of degradation for hormones such as insuhn and aldosterone. In their primary endocrine function, the kidneys produce erythropoietin (EPO), prostaglandins and thromboxanes, renin, and 1,25(0H2)D3. 

Studies of the pathophysiology of acute renal failure has classically considered both tubular and vascular mechanisms [227,228]. In vitro techniques isolating either the vascular or tubular components have been developed. For example, the use of isolated proximal tubules in suspension or in culture allows the study of tubular mechanisms of injury in the absence of vascular factors [229] [230]. There are both in vitro and in vivo models to study vascular injury in the kidney. In vitro models include the study of vascular smooth muscle cells or endothelial cells in culture. In this section, the in vivo methods to evaluate the renal micro-circulation will be discussed. This is of relevance as many nephrotoxins exert their deleterious effects through pharmacologic actions on the resistance vasculature with parenchymal injury occurring as a consequence of ischemia. In clinical practice nephrotoxins may cause prerenal azotemia as a result of increased renal vascular resistance. Nephrotoxins that cause acute renal failure on a vascular basis include prostaglandin inhibitors e.g. aspirin, non-steroidal anti-... 

Most of the renal abnormalities that are clinically encountered as a result of NSAIDs can be attributed to the inhibitory action of these compounds upon prostaglandin production within the kidney. Hence, a brief overview of the influence of prostaglandins on renal function will be presented, followed by an analysis of... 

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