Decreased monosaccharide transport in renal brush-border membrane vesicles of spontaneously hypertensive rats

Mate, Alfonso; Hermosa, M Angeles de la; Barfull, A.; Sánchez‐Aguayo, Inmaculada; Planas, Jordi; Vázquez, Carmen M.

doi:10.1007/s000180050506

Cited by 8 publications

(10 citation statements)

References 23 publications

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“…This study demonstrates that the expression of SGLT2 was not modified in chronic NOS-inhibited hypertensive animals, therefore suggesting that SGLT2 activity is altered in this experimental model. In agreement with these results, Mate et al[ 42] reported a decrease in Na + -glucose uptake in renal BBV from spontaneously hypertensive rats (SHR) compared with control Wistar Kyoto rats. In contrast, Bautista et al [18] described an increase in Na + -dependent D -glucose uptake in renal BBV isolated from rats made hypertensive by aortic coarctation.…”

Section: Discussionsupporting

confidence: 74%

Renal Sodium-Glucose Cotransporter Activity and Aquaporin-2 Expression in Rat Kidney during Chronic Nitric Oxide Synthase Inhibition

et al. 2007

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Background/Aims: The renal sodium glucose cotransporter (SGLT2) and the water channel aquaporin-2 (AQP2) play a critical role in tubular sodium and water reabsorption and in the regulation of extracellular fluid volume both in physiologic and pathophysiologic conditions. However, there is little information about SGLT2 and AQP2 expression and/or activity in hypertension and there are no reports during hypertension induced by chronic nitric oxide synthase (NOS) inhibition. Methods: Hypertension was induced in rats by oral administration of N^G-nitro-L-arginine methyl ester (L-NAME) (20 mg/kg/24 h) for 6 (H6) or 12 (H12) weeks. SGLT2 activity was measured using α-¹⁴C-methylglucose active uptake. The expression level of transporters was assessed by immunohistochemistry and/or immunoblotting. Results: SGLT2 activity was reduced in both H6 and H12; this was due neither to a decrease in SGLT2 expression nor to a change in membrane phospholipid composition. In H6, AQP2 expression diminished only in the inner medulla (IM), while in H12 it diminished in both outer (OM) and IM. This reduced expression of AQP2 may partially account for the increased urinary volume and decreased urinary osmolality in H12, since we obtained a strong correlation between AQP2 expression and these urinary parameters in both OM and IM. Conclusion: We propose that in rats in which hypertension is induced by NOS inhibition, SGLT2 activity and AQP2 expression are modified to compensate for the elevated arterial pressure. However, we cannot discount the possibility that the observed changes are due to the decrease in NO production itself.

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Section: Discussionsupporting

confidence: 74%

Renal Sodium-Glucose Cotransporter Activity and Aquaporin-2 Expression in Rat Kidney during Chronic Nitric Oxide Synthase Inhibition

et al. 2007

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“…In fact, it was recently found that the Na ϩ -dependent D-glucose transport in SHR kidney cortex was significantly lower than in WKY, this being accompanied by similar decreases in the expression of the phlorizin-sensitive D-glucose transporter (31). By contrast, Na ϩ uptake, studied using 22 Na ϩ , was significantly increased in SHR (31). This fits well with the evidence that the hypertensive effect of HS intake on animal models with a diminished renal capacity to excrete salt, such as the SHR (1,4,46), may result from a combination of excessive salt intake and reduced salt excretion (62).…”

Section: Discussionmentioning

confidence: 92%

“…Since increases in blood pressure in hypertensive subjects appear to be linked to an altered Na ϩ transport across the tubular epithelium, as evidenced by increases in the activity of Na ϩ -K ϩ -ATPase (10, 13), type 3 Na ϩ /H ϩ exchanger (NHE3) (29,35,63), and Cl Ϫ /HCO 3 Ϫ exchanger (36), it is likely that in hypertension changes in the Na ϩ transport across the renal tubular epithelium may also affect the Na ϩ -dependent transport of amino acids. In fact, it was recently found that the Na ϩ -dependent D-glucose transport in SHR kidney cortex was significantly lower than in WKY, this being accompanied by similar decreases in the expression of the phlorizin-sensitive D-glucose transporter (31). By contrast, Na ϩ uptake, studied using 22 Na ϩ , was significantly increased in SHR (31).…”

Section: Discussionmentioning

confidence: 94%

High-salt intake and the renal expression of amino acid transporters in spontaneously hypertensive rats

Pinho

Serrão²,

Soares-da-Silva³

2007

American Journal of Physiology-Renal Physiology

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Pinho MJ, Serrão MP, Soares-da-Silva P. High-salt intake and the renal expression of amino acid transporters in spontaneously hypertensive rats. Am J Physiol Renal Physiol 292: F1452-F1463, 2007. First published January 30, 2007 doi:10.1152/ajprenal.00465.2006.-This study evaluated in spontaneously hypertensive rats (SHR) and WistarKyoto rats (WKY) the response to salt loading of the renal dopaminergic system and transcript abundance of Na ϩ -independent (LAT1 and LAT2) and Na ϩ -dependent (ASCT2 and B 0 AT1) amino acid transporters potentially involved in renal tubular uptake of L-DOPA. Rats were fed normal (NS)-or high (HS; 1% saline as drinking water)-salt intake for 24 h. Transcript abundance of amino acid transporters was age dependent, differently regulated in WKY and SHR and responded differently to salt intake. HS intake similarly increased urinary dopamine in 4-wk-old SHR and WKY. At 12 wk of age, HS intake increased urinary dopamine in SHR, but not in WKY. Changes in urinary dopamine paralleled changes in the uptake of L-DOPA in isolated renal tubules from 4-and 12-wk-old WKY and SHR on NS and HS intake. At 12 wk of age, HS intake was accompanied by decreases in LAT1 and LAT2 transcript abundance in WKY and SHR. ASCT2 and B 0 AT1 expression was significantly decreased in both 4-and 12-wk-old WKY and in 4-wk-old SHR on HS intake. By contrast, HS intake increased ASCT2 and B 0 AT1 expression in 12-wk-old SHR. It is concluded that salt-sensitive mechanisms influence LAT1, LAT2, ASCT2, and B 0 AT1 gene transcription. Differences in urinary dopamine and tubular uptake of L-DOPA between WKY and SHR during HS intake, namely in 12-wk-old animals, may result from increases in the ASCT2 and B 0 AT1 mRNA levels and less pronounced decreases in LAT2 expression.LAT2; ASCT2; B 0 AT1; kidney; hypertension THE OCCURRENCE OF HYPERTENSION in humans and laboratory animals is associated with the disruption of normal sodium excretion (7). During moderate salt intake, renal dopamine as a result of D 1 -like receptor activation is responsible for ϳ50% of the sodium excretion (19,37,50). Sodium transport is modulated by renal dopamine, which has its origin in renal proximal tubule (RPT) cells and has been shown to act as an autocrine/paracrine substance (50). Dopamine-induced natriuresis that results from the activation of dopamine D 1 -like receptors is associated with decreases in the activities of the Na ϩ -K ϩ -ATPase and the Na ϩ -H ϩ exchanger (10,15,29,35,63). On the other hand, sodium has been found to constitute an important stimulus for the production of dopamine by RPT cells (53,54,56), resulting in increases in the urinary excretion of dopamine and dopamine metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) (3,14,18,60,61).The spontaneously hypertensive rat (SHR) is the most used experimental model for naturally occurring hypertension, in which salt loading amplifies the structural and functional cardiac and renal changes associated with long-standing hypertension (12). In the SHR, dopa...

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“…Renal cortical BBMVs were prepared from SHR and WKY by a MgCl 2 precipitation method, as previously described in detail [11]. The final pellets containing purified BBMVs were resuspended in the buffers used in transport experiments, whose compositions are reported in uptake studies, and homogenized with a 25-and 29-gauge needle.…”

Section: Preparation Of Bbmvsmentioning

confidence: 99%

“…SGLTs [11]. However, whether the observed changes in the renal transport of D-glucose and D-galactose in hypertensive rats are specific for an Na + -dependent sugar cotransporter or whether other sugar transporters, such as GLUT5, are also affected in the kidney of hypertensive rats is unknown.…”

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confidence: 98%

Characterization of D-fructose transport by rat kidney brush-border membrane vesicles: changes in hypertensive rats

Mate¹,

Hermosa²,

Barfull

et al. 2001

CMLS, Cell. Mol. Life Sci.

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D-fructose transport was characterized in renal brush-border membrane vesicles (BBMVs) from both spontaneously hypertensive rats (SHR) and normotensive genetic control Wistar-Kyoto (WKY) rats. Kinetic studies indicated that the maximal rate (Vmax) of D-fructose transport was significantly lower in SHR compared with WKY rats. No differences were observed in the Michaelis constant (Km) or the diffusion constant (Kd) between the two groups of animals. D-fructose inhibited its own transport, whereas the presence of D-glucose, D-galactose, phlorizin, and cytochalasin B did not inhibit the transport of D-fructose in either animal group. To explain the reduction in D-fructose transport in SHR, the density of the D-fructose transporter, GLUT5, was analyzed by Western blot. GLUT5 levels were lower in SHR, a reduction similar to that of the Vmax. Thus, there appears to be a high-affinity, low-capacity, GLUT5-type fructose carrier in the apical membranes of rat kidney cortex, and the decrease in the Vmax of D-fructose transport in renal BBMVs from hypertensive rats correlates well with a reduction in the expression of GLUT5 protein.

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Decreased monosaccharide transport in renal brush-border membrane vesicles of spontaneously hypertensive rats

Cited by 8 publications

References 23 publications

Renal Sodium-Glucose Cotransporter Activity and Aquaporin-2 Expression in Rat Kidney during Chronic Nitric Oxide Synthase Inhibition

Renal Sodium-Glucose Cotransporter Activity and Aquaporin-2 Expression in Rat Kidney during Chronic Nitric Oxide Synthase Inhibition

High-salt intake and the renal expression of amino acid transporters in spontaneously hypertensive rats

Characterization of D-fructose transport by rat kidney brush-border membrane vesicles: changes in hypertensive rats

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