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      Renal Medullary Infusion of Indomethacin and Adenosine

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          Perfusion of the renal medulla and osmotic hypertonicity of its interstitium are the two important features of this zone which can influence body fluid homeostasis, especially arterial blood pressure. Separate manipulation of the two variables is best obtained with the intramedullary infusion of active agents. In this study, a set-up combining the possibility of infusion into the medulla with measurement of local blood flow (MBF, laser-Doppler flux) and extracellular ion concentration (tissue electrical admittance, Y) was used to determine effects of intramedullary indomethacin (Indo) and adenosine (Ado) in anaesthetized rats. Intramedullary Indo, 1 mg kg<sup>–1 </sup>h<sup>–1</sup>, significantly increased tissue Y, by 12 ± 3%, and significantly decreased MBF by 20 ± 3%.There was also an unexplained increase of sodium excretion (U<sub>Na</sub>V) by 169 ± 24% and of urine flow (V) by 62 ± 6% (n = 10, both p < 0.03). Intramedullary Ado, 5 µg kg<sup>–1</sup> h<sup>–1</sup>, did not alter Y, MBF or U<sub>Na</sub>V, whereas V increased 45 ± 6% and urine osmolality decreased 25 ± 4% (both changes significant). Elevation of medullary interstitial Ado to a level that did not alter MBF or U<sub>Na</sub>V induced a moderate defect of urine concentration that was not due to a decrease in ionic medullary hypertonicity.

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          Cytochrome P450 metabolites of arachidonic acid in the control of renal function.

           K G Maier,  R J Roman (2001)
          Recent studies indicate that arachidonic acid is primarily metabolized by cytochrome P450 enzymes of the 4A and 2C families in the kidney to 20-hydroxyeicosatetraenoic acid (HETE), epoxyeicosatrienoic acids (EETs) and dihydroxyeicosatrienoic acids. These compounds play central roles in the regulation of renal tubular and vascular function. 20-HETE is produced by renal vascular smooth muscle (VSM) cells and is a potent constrictor that depolarizes VSM cells by blocking the calcium-activated potassium channel. Inhibition of the formation of 20-HETE blocks the myogenic response of isolated renal arterioles in vitro, and autoregulation of renal blood flow and tubuloglomerular feedback responses in vivo. EETs are products formed in the endothelium and are potent dilators that activate the calcium-activated potassium channel in renal VSM. Endothelial-dependent vasodilators stimulate the release of EETs, and these compounds appear to serve as an endothelial-derived hyperpolarizing factor. EETs and 20-HETE are produced in the proximal tubule. There, they regulate sodium/potassium-ATPase activity and serve as second messengers for the natriuretic effects of dopamine, parathyroid hormone and angiotensin II. 20-HETE is also produced in the thick ascending loop of Henle. It regulates sodium-potassium-chloride transport in this nephron segment. The renal production of cytochrome P450 metabolites of arachidonic acid is altered in hypertension, diabetes, toxemia of pregnancy, and hepatorenal syndrome. Given the importance of cytochrome P450 metabolites of arachidonic acid in the control of renal function, it is likely that changes in this system contribute to the abnormalities in renal function that are associated with many of these conditions.
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            Prostaglandin E2 induced changes in renal blood flow, renal interstitial hydrostatic pressure and sodium excretion in the rat

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              Osmotic hypertonicity of the renal medulla during changes in renal perfusion pressure in the rat


                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                July 2004
                02 February 2004
                : 27
                : 1
                : 29-34
                Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland
                75620 Kidney Blood Press Res 2004;27:29–34
                © 2004 S. Karger AG, Basel

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                Figures: 3, References: 27, Pages: 6
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