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Renal Medulla (renal + medulla)
Selected AbstractsEndothelin regulates NOS1 and NOS3 isoforms in the renal medullaACTA PHYSIOLOGICA, Issue 4 2007Erik Persson No abstract is available for this article. [source] Endothelin receptor selectivity in chronic kidney disease: rationale and review of recent evidenceEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2009W. Neuhofer Abstract Endothelin (ET) is a potent vasoconstrictory peptide with proinflammatory and profibrotic properties that exerts its biological effects through two pharmacologically distinct receptor subtypes, namely ETA and ETB. In addition to its substantial contribution to normal renal function, a large body of evidence suggests that derangement of the renal ET system is involved in the initiation and progression of chronic kidney disease (CKD) in diabetes, hypertension and glomerulonephritis. Thus, the use of ET receptor antagonists (ERAs) may offer potential novel treatment strategies in CKD. Recent literature on the role of the renal ET system in the healthy kidney was reviewed. In addition, an unbiased PubMed search was performed for studies published during the last 5 years that addressed the effects of ERAs in CKD. A particular objective was to extract information regarding whether selective or nonselective ERAs may have therapeutic potential in humans. ET-1 acts primarily as an autocrine or paracrine factor in the kidney. In normal physiology, ET-1 promotes diuresis and natriuresis by local production and action through ETB receptors in the renal medulla. In pathology, ET-1 mediates vasoconstriction, mesangial-cell proliferation, extracellular matrix production and inflammation, effects that are primarily conveyed by ETA receptors. Results obtained in animal models and in humans with the use of ERAs in CKD are encouraging; nevertheless, it is still under debate which receptor subtype should be targeted. According to most studies, selective inhibition of ETA receptors appears superior compared with nonselective ERAs because this approach does not interfere with the natriuretic, antihypertensive and ET clearance effects of ETB receptors. Although preliminary data in humans are promising, the potential role of ERAs in patients with CKD and the question of which receptor subtype should be targeted can only be clarified in randomized clinical trials. [source] Role of nitric oxide in the reflex diuresis in rabbits during pulmonary lymphatic obstructionEXPERIMENTAL PHYSIOLOGY, Issue 4 2004K. M. McCormick The role of nitric oxide in the reflex diuresis in response to pulmonary lymphatic drainage was examined in anaesthetized, artificially ventilated New Zealand White rabbits. Pulmonary lymphatic drainage was obstructed by raising the pressure in a pouch created from the right external jugular vein. Pulmonary lymphatic obstruction resulted in a significant increase in urine flow from an initial control value of 8.9 ± 0.5 ml (10 min),1 to 12.1 ± 0.6 ml (10 min),1 during lymphatic obstruction (mean ±s.e.m.; n= 17, P < 0.001). This increase in urine flow was accompanied by a significant increase in the excretion of sodium. Additionally, renal blood flow remained unchanged during the increase in urine flow caused by lymphatic obstruction. Intravenous infusion of l -NAME, a non-selective inhibitor of nitric oxide synthase (NOS), abolished the reflex diuresis. Furthermore, intraperitoneal administration of the relatively selective neuronal NOS blocker, 7-nitroindazole also abolished the response. It was observed that infusion of a more soluble neuronal NOS blocker, 7-nitroindazole sodium salt (7-NINA), into the renal medulla also abolished the reflex diuresis. These findings suggest that the increase in urine flow in rabbits caused by pulmonary lymphatic obstruction is dependent upon the integrity of neuronal NOS activity within the renal medulla. [source] Spoke-wheel-like enhancement as an important imaging finding of chromophobe cell renal carcinoma: A retrospective analysis on computed tomography and magnetic resonance imaging studiesINTERNATIONAL JOURNAL OF UROLOGY, Issue 10 2004TSUNENORI KONDO Abstract Aim:, Little information has been reported with regard to the radiological features of chromophobe cell renal carcinomas (CCRC). The aim of the present study was to identify imaging characteristics which lead to the histological diagnosis of CCRC. Methods:, The imaging findings of computed tomography (CT) and magnetic resonance imaging (MRI) were retrospectively analyzed in 11 patients with CCRC operated on at Tokyo Women's Medical University, Tokyo, Japan. Results:, None of the factors studied were significant in distinguishing the two variants, typical and eosinophilic variants. Enhanced CT scans showed a spoke-wheel-like enhancement with a central scar in 3 patients (27%). The radiological patterns were classified into two groups. Seven patients (64%) showed pattern 1 in which: (i) a hypodense to isodense enhancement compared to the renal medulla in the corticomedullary phase during dynamic CT; (ii) an isodense mass compared to the renal medulla in unenhanced CT scan; and (iii) a lobulated appearance were typically observed. Four patients (36%) showed pattern 2 that seemed to be similar to the features of clear cell carcinoma, having an alveolar structure including a hyperdense enhancement in the corticomedullary phase and an inhomogeneous appearance. A spoke-wheel-like enhancement was observed only in patients with pattern 1, and was more clearly demonstrated in larger tumors. Conclusions:, The CT and MRI findings in CCRC patients were not uniform, but it was noted that a spoke-wheel-like enhancement with a central stellate scar, which might have been mistaken for oncocytoma, was one of important findings of CCRC. Tumors demonstrating a spoke-wheel-like enhancement with a central scar should be carefully managed, because they could be malignant. [source] Insulin alters cytokine content in two pivotal organs after brain death: a porcine modelACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2008A. BARKLIN Background: To optimize the quantity and quality of organs available for transplantation, it is crucial to gain further insight into the treatment of brain dead organ donors. In the current study we hypothesized that insulin treatment after brain death alters cytokine content in the heart, liver, and kidney. Methods: Sixteen brain dead pigs (35,40 kg) were treated with either (1) no insulin [brain dead without insulin treatment treatment (BD)], or (2) insulin infusion intravenously (i.v.) at a constant rate of 0.6 mU/kg/min during 360 min [brain dead with insulin treatment (BD+I)]. Blood glucose was clamped at 4.5 mmol/l by infusion of 20% glucose. Blood samples for insulin, glucose, catecholamines, free fatty acids, and glucagon were obtained during the experimental period. Six hours after brain death biopsies were taken from the heart, liver, and kidney. These were analyzed for cytokine mRNA and proteins [tumor necrosis factor-, (TNF-,), interleukin (IL)-6, and IL-10]. Results: The BD+I compared with the BD animals had lower IL-6 concentrations in the right ventricle of the heart (P=0.001), in the renal cortex (P=0.04) and in the renal medulla (P=0.05), and lower IL-6 mRNA in the renal medulla (P=0.0002). Furthermore, the BD+I animals had lower concentrations in the renal medulla of IL-10 (P=0.01), and tended to have lower TNF-, in the renal cortex (P=0.06) than the BD animals. In the right ventricle of the heart TNF-, mRNA and IL-10 mRNA were higher in the BD+I than in the BD group (P=0.002 and 0.004). Conclusion: Insulin has anti-inflammatory effects on cytokine concentration in the heart and kidney after brain death. [source] Imaging the changes in renal T1 induced by the inhalation of pure oxygen: A feasibility studyMAGNETIC RESONANCE IN MEDICINE, Issue 4 2002Richard A. Jones Abstract The effect of the inhalation of pure oxygen on the kidney was evaluated by measuring monoexponential T1 and T relaxation times in nine volunteers using a multiple-shot turbo spin echo and multiple echo gradient echo sequences, respectively. The T1 of the renal cortex decreased significantly when breathing pure oxygen as compared to normoxia (from 882 ± 59 to 829 ± 70 msec, P < 0.05), while that of the renal medulla was unchanged. No significant changes were seen in the T of either compartment. Dynamic imaging using an inversion recovery sequence with an optimized inversion time typically produced signal changes of 20% in the renal cortex. Studies to assess if oxygen-induced changes in flow contributed to this effect showed that the flow contribution was not significant. Although longer inversion times (880 ms) produced optimal contrast, acceptable contrast was also obtained at shorter inversion times (450 msec) in the renal cortex, spleen, and lung, with the latter being of opposite polarity to the other two tissues, implying a shorter parenchymal T1 than previously reported in the literature. The results are consistent with oxygen acting as an intravascular contrast agent which induces a shortening of T1 in the arterial blood volume. Magn Reson Med 47:728,735, 2002. © 2002 Wiley-Liss, Inc. [source] Nitric oxide synthesis and nitric oxide synthase expression in the kidney of rats treated by FK506NEPHROLOGY, Issue 1 2002LiMing WANG SUMMARY: FK506-induced nephrotoxicity is characterized by a disturbance in renal haemody-namics that is attributed to an imbalance between the various modulators of renal vascular tone. It has not been well defined whether nitric oxide (NO), as an important vasoactive factor, is involved in FK506-induced nephrotoxicity. This study was designed to evaluate the involvement of nitric oxide in FK506-induced nephrotoxicity by investigating NO synthesis and NO synthase (NOS) expression in the kidney of rats treated with FK506. Male Wistar rats weighing 240,260 g, aged 11 weeks, were administered with FK506 (3.2mg/kg per day i.m.) for 4 weeks. Renal function and urinary NOx was measured using biochemical methods at the end of both 2 and 4 weeks of treatment. Expression of NOS protein and NOS mRNA in the kidney was also investigated using Western blot analysis and reverse transcription/polymerase chain reaction, respectively. FK506 administration induced nephrotoxicity, which was indicated by renal dysfunction (elevated blood urea nitrogen and creatinine, and reduced creatinine clearance, P < 0.05 vs control). FK506-induced nephrotoxicity was accompanied by higher urinary NOx excretion at the end of 2 weeks' treatment. In parallel with an increase in NO synthesis, increased eNOS protein and mRNA expression were also found in the renal medulla and renal cortex at week 2. the expression remained at higher levels in the renal medulla and returned to normal levels in the renal cortex at week 4. FK506 treatment induced nephrotoxicity in rats, which was accompanied by a temporal increase in NO synthesis in the kidney. Increased eNOS protein and mRNA expression were also found in the kidney of treated rats, which may be responsible for the enhanced NO synthesis. [source] Protective Effects of Glycyrrhizin on Gentamicin-Induced Acute Renal Failure in RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2003Eun-Jin Sohn Polyuria in rats with gentamicin-induced acute renal failure was associated with down-regulation of renal aquaporin 2 in the inner and outer renal medulla, and cortex. Glycyrrhizin administration restored the expression of aquaporin 2 with paralleled changes in urine output. Changes in renal functional parameters, such as creatinine clearance, urinary osmolality, and solute-free reabsorption, accompanying acute renal failure were also partially restored after administration of glycyrrhizin. Histological changes in rats with gentamicin-induced acute renal failure were also abrogated by glycyrrhizin treatment. The above results suggest that glycyrrhizin treatment could ameliorate renal defects in rats with acute renal failure induced by gentamicin. [source] MECHANISMS MEDIATING PRESSURE NATRIURESIS: WHAT WE KNOW and WHAT WE NEED TO FIND OUTCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2005Roger G Evans SUMMARY 1.,It is well established that pressure natriuresis plays a key role in long-term blood pressure regulation, but our understanding of the mechanisms underlying this process is incomplete. 2.,Pressure natriuresis is chiefly mediated by inhibition of tubular sodium reabsorption, because both total renal blood flow and glomerular filtration rate are efficiently autoregulated. Inhibition of active sodium transport within both the proximal and distal tubules likely makes a contribution. Increased renal interstitial hydrostatic pressure (RIHP) likely inhibits sodium reabsorption by altering passive diffusion through paracellular pathways in ,leaky' tubular elements. 3.,Nitric oxide and products of cytochrome P450-dependent arachidonic acid metabolism are key signalling mechanisms in pressure natriuresis, although their precise roles remain to be determined. 4.,The key unresolved question is, how is increased renal artery pressure ,sensed' by the kidney? One proposal rests on the notion that blood flow in the renal medulla is poorly autoregulated, so that increased renal artery pressure leads to increased renal medullary blood flow (MBF), which, in turn, leads to increased RIHP. An alternative proposal is that the process of autoregulation of renal blood flow leads to increased shear stress in the preglomerular vasculature and, so, release of nitric oxide and perhaps products of cytochrome P450-dependent arachidonic acid metabolism, which, in turn, drive the cascade of events that inhibit sodium reabsorption. 5.,Central to the arguments underlying these opposing hypotheses is the extent to which MBF is autoregulated. This remains highly controversial, largely because of the limitations of presently available methods for measurement of MBF. [source] Changes in mean arterial pressure predict degranulation of renomedullary interstitial cellsCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2002Christine Maric Summary 1.,Renomedullary interstitial cells (RMIC) are characterized by numerous intracellular granules thought to contain renal medullary antihypertensive substances. However, the nature of the trigger for RMIC degranulation remains to be elucidated. The present study examines the effects of acute alterations in mean arterial pressure (MAP) and medullary blood flow (MBF) on RMIC granulation. 2.,Basal MAP and MBF in anaesthetized Sprague-Dawley rats (n = 4/group) were altered by intravenous infusions of vasoactive agents, including angiotensin II alone or with a nitric oxide (NO) synthase inhibitor (N, -nitro- l -arginine) or NO donor (sodium nitroprusside), noradrenaline and by carotid artery clamping. Following these treatments, kidneys were examined by electron microscopy and the absolute volume of granules in the renal medulla was calculated using unbiased stereological methods. 3.,Acute increases in MAP, regardless of the treatment causing the increase, were associated with a reduction in the absolute volume of granules in the range of 42,67%. Regression analysis revealed that only increases in MAP, but not MBF, strongly predict RMIC degranulation. 4.,Despite previous reports that changes in MBF activate renomedullary antihypertensive activity, we conclude that the change in MAP is an important determinant of the activity of the blood pressure-lowering mechanism of the renal medulla, with the assumption that the medullary lipids mediate the antihypertensive property of the renal medulla. [source] | |||||||||||||