Renal haemodynamic and tubular actions of urotensin II in the rat

Abdel-Razik, AE; Forty, Ellen; Balment, R. J.; Ashton, Nick

doi:10.1677/joe-08-0260

Cited by 19 publications

(30 citation statements)

References 33 publications

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“…Rat UII infusion rates (0.6 pmol or 6 pmol⅐min Ϫ1 ⅐100 g body wt Ϫ1 ) were chosen, on the basis of earlier studies in our laboratory (1,30), to induce modest, physiologically relevant changes in plasma UII concentrations with no accompanying alterations in systemic blood pressure. This aim was achieved as rUII infusion had no effect on mean arterial pressure (MAP) at either dose in both SHR (P treatment ϭ 0.47) and WKY (P treatment ϭ 0.41) rats (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…This pattern of distribution is in agreement with our observations of the profound effects of UII on renal hemodynamic and tubular function in the rat in vivo. UII administration caused a marked reduction in glomerular filtration rate (GFR) which was accompanied by an antidiuresis and antinatriuresis (1,30). Other groups (24,36) reported somewhat different effects, perhaps reflecting different doses and/or routes of UII administration, but nonetheless showed that UII can influence both glomerular filtration and tubular sodium reabsorption.…”

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confidence: 99%

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Enhanced renal sensitivity of the spontaneously hypertensive rat to urotensin II

Abdel-Razik¹,

Balment²,

Ashton³

2008

American Journal of Physiology-Renal Physiology

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Abdel-Razik AE, Balment RJ, Ashton N. Enhanced renal sensitivity of the spontaneously hypertensive rat to urotensin II. Am J Physiol Renal Physiol 295: F1239 -F1247, 2008. First published August 13, 2008 doi:10.1152/ajprenal.90374.2008.-Urotensin II (UII) has been implicated widely in cardiovascular disease. The mechanism(s) through which it contributes to elevated blood pressure is unknown, but its emerging role as a regulator of mammalian renal function suggests that the kidney might be involved. The aim of this study was to determine the effect of UII on renal function in the spontaneously hypertensive rat (SHR). UII infusion (6 pmol ⅐ min Ϫ1 ⅐ 100 g body wt Ϫ1 ) in anesthetized SHR and control Wistar-Kyoto (WKY) rats produced marked reductions in glomerular filtration rate (⌬GFR WKY, n ϭ 7, Ϫ0.3 Ϯ 0.1 vs. SHR, n ϭ 7, Ϫ0.6 Ϯ 0.1 ml ⅐ min Ϫ1 ⅐ 100 g body wt Ϫ1 , P ϭ 0.03), urine flow, and sodium excretion rates, which were greater in SHR by comparison with WKY rats. WKY rats also showed an increase in fractional excretion of sodium (⌬FENa; ϩ0.6 Ϯ 0.1%, P ϭ 0.02) in contrast to SHR in which no such change was observed (⌬FENa Ϫ0.6 Ϯ 0.2%). Blockade of the UII receptor (UT), and thus endogenous UII activity, with urantide evoked an increase in GFR which was greater in SHR (ϩ0.3 Ϯ 0.1) compared with WKY rats (ϩ0.1 Ϯ 0.1 ml ⅐ min Ϫ1 ⅐ 100 g body wt Ϫ1 , P ϭ 0.04) and was accompanied by a diuresis and natriuresis. UII and UT mRNA expression were greater in the renal medulla than the cortex of both strains; however, expression levels were up to threefold higher in SHR tissue. SHR are more sensitive than WKY to UII, which acts primarily to lower GFR thus favoring salt retention in this model of hypertension.UT receptor; kidney; glomerular filtration rate; sodium THE NOVEL PEPTIDE hormone urotensin II (UII), originally identified in a neurohemal organ unique to fish (3), is now known to be expressed in many mammalian species, including humans (9) and rats (8). UII binds to a single specific G protein-coupled receptor (2, 18), designated the UT receptor (11), which is expressed abundantly in the nervous (13) and cardiorenal systems (20,30). The potent vasoconstrictor actions of UII (2) appear to be mediated by Ca 2ϩ mobilization through activation of a number of signaling pathways, including Ca 2ϩ channels, tyrosine kinase, p38MAPK, and ERK1/2 (26). UII also has a vasodepressor action, particularly in the rat, which is endothelium and nitric oxide dependent (26).UII has been implicated widely in cardiovascular disease. Plasma (7) and cerebrospinal fluid (31) UII concentrations have been positively correlated with blood pressure in hypertensive patients and single nucleotide polymorphisms of the UII gene have been associated with the development of essential hypertension (35). Elevated plasma or urinary UII concentrations have also been reported in patients with portal hypertension (15), congestive heart failure (22, 27), and renal failure (21, 32). These observations led to the suggestion that UII plays a role in card...

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Enhanced renal sensitivity of the spontaneously hypertensive rat to urotensin II

Abdel-Razik¹,

Balment²,

Ashton³

2008

American Journal of Physiology-Renal Physiology

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“…Both unglycosylated (w42 kDa) and glycosylated (w60 kDa) forms of UTR protein have been identified in human adrenocortical tissues and COS-7 cells overexpressing UTR (Boucard et al 2003, Giuliani et al 2009). Ventricular samples from rats express the unglycosylated form of UTR, whereas the glycosylated form was the only immunoreactive UTR protein identified in rat kidneys, coronary arteries, and cultured coronary artery smooth muscle cells (Gong et al 2004, Abdel-Razik et al 2008b, DominguezRodriguez et al 2012. In this study, we found that newborn pig renal afferent arterioles express both unglycosylated and glycosylated forms of UTR.…”

Section: Discussionmentioning

confidence: 99%

Pressor and renal regional hemodynamic effects of urotensin II in neonatal pigs

Soni¹,

Adebiyi²

2013

Journal of Endocrinology

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Renal expression of the peptide hormone urotensin II (UII) and its receptor (UTR) are dependent on kidney maturation and anatomical regions. However, renal regional hemodynamic effects of UII in neonates are unclear. Here, we investigated regional hemodynamic responses to acute intrarenal arterial administration of UII in newborn pigs. Western immunoblotting and immunofluorescence confirmed UTR expression and membrane localization in newborn pig renal afferent arterioles and afferent arteriolar smooth muscle cells respectively. Intrarenal arterial bolus injections of human UII (hUII; 1-100 ng/kg) resulted in a dose-dependent decrease in total renal blood flow (RBF) and an increase in mean arterial pressure (MAP) and renal vascular resistance (RVR) in newborn pigs. Moreover, hUII dose dependently reduced cortical blood flow (CBF) but increased medullary blood flow (MBF) in the piglets. hUII-induced MAP elevation and hemodynamic changes were inhibited by urantide, a UTR antagonist, but not losartan, a type 1 angiotensin II receptor antagonist. U-73122, a phospholipase C (PLC) inhibitor, and 2-aminoethoxydiphenyl borate, an inositol 1,4,5 trisphosphate (IP 3 ) receptor antagonist, attenuated hUII-induced MAP and RVR elevations, RBF and CBF reductions, but not MBF increase. These findings indicate that intrarenal arterial administration of hUII elevates blood pressure and induces region-selective renal hemodynamic changes in newborn pigs. Our data also suggest that the PLC/IP 3 signaling pathway contributes to hUII-induced alterations in MAP, RBF, RVR, and CBF but not MBF in newborn pigs.

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“…injection of iron into rats and mice resulted in iron-induced free radical injury and cancer in the kidney. 46 Renal tissue Ang II concentration has been reported to be 5.8 nmol kg -1 kidney wt, 47 which is two orders higher than the serum Ang II level. First, we analyzed whether Ang II treatment increases intracellular iron concentration.…”

Section: Effect Of Ang II On Iron-transporting Protein S Tajima Et Almentioning

confidence: 97%

Effect of angiotensin II on iron-transporting protein expression and subsequent intracellular labile iron concentration in human glomerular endothelial cells

et al. 2010

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Angiotensin II (Ang II)-induced endothelial injury, which is associated with atherosclerosis, is believed to be mediated by intracellular reactive oxygen species (ROS) through stimulation of nicotinamide adenine dinucleotide phosphate oxidase (NOX). Iron is essential for the amplification of oxidative stress. In this study, we investigated whether Ang II altered iron metabolism and whether the Ang II-induced endothelial injury is attributable to changes in iron metabolism of human glomerular endothelial cells (HGECs). When 90% iron-saturated human transferrin (90% Tf) was applied to HGECs without Ang II, the labile ferrous iron level was same as the effect of control in spite of a significant increase in the total cellular iron concentration. Treatment with Ang II and 30% Tf or 90% Tf significantly (Po0.01) increased the intracellular iron concentration, as well as labile ferrous iron and protein oxidation levels, compared with the effect of separate administration of each compound. Ang II treatment facilitated the protein expression of the Tf receptor, divalent metal transporter 1, and ferroportin 1 in a dose-and timedependent manner. It was also found that simultaneous exposure of HGECs to Ang II and 90% Tf accelerated hydroxyl radical production, as shown by using an electron paramagnetic resonance spectrometer. These results suggest that Ang II not only induces production of ROS by NOX activation but also iron incorporation followed by an increase in labile iron in HGECs. Both of these events may participate in the progression of oxidative stress because of endothelial cell dysfunction through ferrous iron-mediated ROS generation.

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Renal haemodynamic and tubular actions of urotensin II in the rat

Cited by 19 publications

References 33 publications

Enhanced renal sensitivity of the spontaneously hypertensive rat to urotensin II

Enhanced renal sensitivity of the spontaneously hypertensive rat to urotensin II

Pressor and renal regional hemodynamic effects of urotensin II in neonatal pigs

Effect of angiotensin II on iron-transporting protein expression and subsequent intracellular labile iron concentration in human glomerular endothelial cells

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