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Inner Medulla (inner + medulla)
Selected AbstractsEndothelinA (ETA) and ETB receptor-mediated regulation of nitric oxide synthase 1 (NOS1) and NOS3 isoforms in the renal inner medullaACTA PHYSIOLOGICA, Issue 4 2007J. C. Sullivan Abstract Aim:, Our laboratory and others have shown that endothelin (ET)-1 directly stimulates nitric oxide (NO) production in inner medullary collecting duct (IMCD) cells. The goal of this study was to determine which NO synthase (NOS) isoforms in IMCD are sensitive to ET-1, and the role of ETA and ETB receptor activation in vivo and in vitro. Methods:, NOS enzymatic activity and NOS isoform protein expression were examined in cultured IMCD-3 cells and isolated renal inner medulla. ETB receptor-deficient homozygous rats (sl/sl) have elevated levels of circulating ET-1 and lack a functional ETB signalling pathway in kidneys, and furthermore provides a unique model to study ETA receptor signalling in the renal inner medulla in vivo. Results:, Incubation of IMCD-3 cells with exogenous ET-1 (50 nm) resulted in ETA -dependent increased NOS1 protein expression in IMCD-3 cells with no effect on NOS2 or NOS3 expression. ETB receptor antagonism has no effect on NOS expression in IMCD-3 cells. Consistent with in vitro results, cytosolic NOS1 protein expression was significantly greater in the renal inner medulla of sl/sl rats compared with heterozygous (sl/+) controls, with no alteration in NOS3 expression. In contrast to protein expression data, NOS1- and NOS3-specific enzymatic activities decreased in the cytosolic fraction from the renal inner medulla of sl/sl compared with sl/+. Conclusion:, These results provide evidence that both ETA and ETB receptors regulate NOS isoform activity in the renal inner medulla and specifically support the hypothesis that ETA receptor activation increases NOS1 expression. [source] Vacuolar H+ -ATPase expression is increased in acid-secreting intercalated cells in kidneys of rats with hypercalcaemia-induced alkalosisACTA PHYSIOLOGICA, Issue 4 2007W. Wang Abstract Aims:, Hypercalcaemia is known to be associated with systemic metabolic alkalosis, although the underlying mechanism is uncertain. Therefore, we aimed to examine whether hypercalcaemia was associated with changes in the expression of acid,base transporters in the kidney. Methods:, Rats were infused with human parathyroid hormone (PTH, 15 ,g kg,1 day,1), or vehicle for 48 h using osmotic minipumps. Results:, The rats treated with PTH developed hypercalcaemia and exhibited metabolic alkalosis (arterial HCO: 31.1 ± 0.8 vs. 28.1 ± 0.8 mmol L,1 in controls, P < 0.05, n = 6), whereas the urine pH of 6.85 ± 0.1 was significantly decreased compared with the pH of 7.38 ± 0.1 in controls (P < 0.05, n = 12). The observed alkalosis was associated with a significantly increased expression of the B1-subunit of the H+ -ATPase in kidney inner medulla (IM, 233 ± 45% of the control level). In contrast, electroneutral Na+ -HCO cotransporter NBCn1 and Cl,/HCO anion exchanger AE2 expression was markedly reduced in the inner stripe of the outer medulla (to 26 ± 9% and 65 ± 6%, respectively). These findings were verified by immunohistochemistry. Conclusions:, (1) hypercalcaemia-induced metabolic alkalosis was associated with increased urinary excretion of H+; (2) the increased H+ -ATPase expression in IM may partly explain the enhanced urinary acidification, which is speculated to prevent stone formation because of hypercalciuria and (3) the decreased expression of outer medullary AE2 suggests a compensatory reduction of the transepithelial bicarbonate transport. [source] Evaluation of intrarenal oxygenation in mice by BOLD MRI on a 3.0T human whole-body scanner,JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 3 2007Lu-Ping Li PhD Abstract Purpose To extend observations on intra-renal oxygenation with blood oxygen level-dependent (BOLD) MRI in human and rats to mouse kidneys imaged with a human whole-body scanner. Materials and Methods Renal BOLD MRI studies were performed on a 3.0T scanner using a multiple gradient-echo (mGRE) sequence with a custom-designed 2.0-cm surface coil to acquire six T2*-weighted images in mice (N = 8) at an in-plane resolution of 156 × 156 ,m2. BOLD MRI data were obtained before and after administration of furosemide (10 mg/kg intravenously [i.v.]). Results The mean weight of eight mice was 24.6 ± 1.0 g. The baseline renal R2* (mean ± standard error [SE]) was 28.6 ± 2.1 seconds,1 in the renal cortex (CO), 35.4 ± 2.2 in the outer medulla (OM), and 21.2 ± 2.1 seconds,1 in the inner medulla (IM). The BOLD response to furosemide (,R2*) was 4.1 ± 1.4 in the CO, 10.1 ± 2.1 seconds,1 in the OM, and 3.4 ± 0.8 seconds,1 in the IM in mice. Conclusion Intrarenal BOLD MR images with sufficiently high resolution can be obtained on a human whole-body scanner when combined with a small receiver coil to allow studies in mice. Both baseline R2* and ,R2* values following administration of furosemide were consistent with previous experience in humans and rats. J. Magn. Reson. Imaging 2007. © 2007 Wiley-Liss, Inc. [source] Differential action of bradykinin on intrarenal regional perfusion in the rat: waning effect in the cortex and major impact in the medullaTHE JOURNAL OF PHYSIOLOGY, Issue 15 2009ena B The renal kallikrein,kinin system is involved in the control of the intrarenal circulation and arterial pressure but bradykinin (Bk) effects on perfusion of individual kidney zones have not been examined in detail. Effects of Bk infused into renal artery, renal cortex or medulla on perfusion of whole kidney (RBF, renal artery probe) and of the cortex, outer- and inner medulla (CBF, OMBF, IMBF: laser-Doppler fluxes), were examined in anaesthetized rats. Renal artery infusion of Bk, 0.3,0.6 mg kg,1 h,1, induced no sustained increase in RBF or CBF. OMBF and IMBF increased initially 6 or 16%, respectively; only the IMBF increase (+10%) was sustained. Pre-treatment with l -NAME, 2.4 mg kg,1i.v., prevented the sustained but not initial transient elevation of medullary perfusion. Intracortical Bk infusion, 0.75,1.5 mg kg,1 h,1, did not alter RBF or CBF but caused a sustained 33% increase in IMBF. Intramedullary Bk, 0.3 mg kg,1 h,1, did not alter RBF or CBF but caused sustained increases in OMBF (+10%) and IMBF (+23%). These responses were not altered by pre-treatment with 1-aminobenzotriazole, 10 mg kg,1i.v., a cytochrome P-450 (CYP450) inhibitor, but were prevented or significantly attenuated by l -NAME or intramedullary clotrimazole, 3.9 mg kg,1 h,1, an inhibitor of CYP450 epoxygenase and of calcium-dependent K+ channels (KCa). Thus, cortical vasodilatation induced by Bk is only transient so that the agent is unlikely to control perfusion of the cortex. Bk selectively increases perfusion of the medulla, especially of its inner layer, via activation of the NO system and of KCa channels. [source] | ||||||||||