Erythrocyte Na+‐H+ exchanger and Na+‐Li+ countertransport activity in primary aldosteronism

Delva, Pietro; Pastori, Caterina; Degan, Maurizio; Montesi, Germana; Bassi, Antonella; Lechi, Alessandro

doi:10.1111/j.1365-2362.1994.tb02021.x

Cited by 9 publications

(3 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The parallel extrusion of H + by the Na + /H + exchanger and of HCO 3 - by the Cl - /HCO 3 - exchanger is osmotically not relevant, as H + and HCO 3 - are replenished in the cell from CO 2 via H 2 CO 3 [92,94]. Aldosterone is known to upregulate the Na + /H + exchanger in the kidney [95,96], heart [97,98,99], and several additional tissues [100,101,102,103,104,105,106,107,108,109,110]. Whether or not pendrin participates in platelet cell volume regulation, remains, however, to be shown.…”

Section: Discussionmentioning

confidence: 99%

Sgk1 Sensitive Pendrin Expression in Murine Platelets

Pelzl

Fakhri²,

Umbach³

et al. 2013

Cell Physiol Biochem

View full text Add to dashboard Cite

Background: The anion exchanger pendrin (SLC26A4) is required for proper development of the inner ear, and contributes to iodide organification in thyroid glands as well as anion transport in various epithelia, such as airways and renal tubules. SLC26A4 deficiency leads to Pendred syndrome, which is characterized by hearing loss with enlarged vestibular aqueducts and variable hypothyroidism and goiter. Pendrin expression in kidney, heart, lung and thyroid is up-regulated by the mineralocorticoid deoxycorticosterone (DOCA). Platelets express anion exchangers but virtually nothing is known about the molecular identity and regulation of those carriers. Other carriers such as the Na⁺/H⁺ exchanger are regulated by the mineralocorticoid-sensitive serum and glucocorticoid inducible kinase SGK1. Methods: The present study utilized i) quantitative reverse transcription polymerase chain reaction (RT-qPCR) to quantify the transcript levels of Slc26a4 as compared to Gapdh and ii) western blotting to assess Slc26a4 protein abundance in murine platelets from gene-targeted mice lacking Sgk1 (sgk1^-/-) and respective wild type animals (sgk1^+/+) treated without or with a subcutaneous injection of 2.5 mg DOCA for 3 h, or in sgk1^+/+ platelets with or without in vitro treatment for 1 h with 10 µg/ml DOCA. Results: Slc26a4 was expressed in platelets, and in vitro DOCA treatment increased Slc26a4 mRNA levels in platelets isolated from sgk1^+/+ mice. Moreover, in vivo DOCA treatment significantly up-regulated Slc26a4 mRNA levels in platelets isolated from sgk1^+/+ but not sgk1^-/- mice. An increase in Sgk1 mRNA levels paralleled that of Slc26a4 mRNA levels in platelets of sgk1^+/+ mice. In addition, DOCA treatment further increased Slc26a4 protein abundance in platelets isolated from sgk1^+/+ mice. Conclusions: Pendrin is expressed in platelets and is presumably regulated by SGK1 and mineralocorticoids.

show abstract

Section: Discussionmentioning

confidence: 99%

Sgk1 Sensitive Pendrin Expression in Murine Platelets

Pelzl

Fakhri²,

Umbach³

et al. 2013

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…LNE seems to be increased only among essential hypertensives. It was evaluated among patients with primary aldosteronism, estrogen-induced hypertension, polycystic kidney disease, renovascular hypertension, chronic glomerulonephritis, lupus erythematosus, and endstage renal disease with negative results (9,36,(90)(91)(92)(93). In pigs, however, it has been shown that deoxycosterone acetate treatment may simultaneously increase blood pressure and red-cell LNE (94).…”

Section: Lne In Secondary Hypertension and Other Clinical Conditionsmentioning

confidence: 99%

The Li sup sup Na sup nbsp sup exchange in hypertension

Semplicini

Sartori²,

Ceolotto³

et al. 2003

Front Biosci

View full text Add to dashboard Cite

The red cell membrane Li+/Na+exchange is a heteroexchange that operates in either direction across the cell membrane. It binds either Li+ or Na+ on one side of the membrane and it exchanges the transported species for either Li+ or Na+ on the opposite side in a stoichiometric ratio of 1:1. In the population, Li+/Na+exchange is unimodally distributed but skewed to the right. Such distribution results from superimposition of two normal distributions. Many laboratories have shown that red-cell Li+/Na+ exchange is increased in patients with essential hypertension, compared with normotensive controls. Among the various alterations of cell membrane cation transport reported in hypertension, the increase of red-cell Li+/Na+ exchange has been most widely investigated and confirmed. Moreover, increased Li+/Na+ exchange has been found in some clinical conditions related to hypertension, such as overweight and diabetes. Among diabetic patients, Li+/Na+ exchange is particularly high in patients with nephropathy, hypertension, and microalbuminuria, leading to the hypothesis that it can be considered a cellular marker of the risk of developing diabetic nephropathy. Furthermore, it is associated with severe and drug-resistant hypertension, insulin resistance, vascular and cardiac hypertrophy, hyperlipidemia, obesity, family history of hypertension, and of major cardiovascular accidents suggesting that high Li+/Na+ exchange could be a biochemical marker for increased cardiovascular risk. Regardless of its the pathophysiological significance, its measurement could be of clinical use as an intermediate phenotype of increased cardiovascular risk.

show abstract

“…Furthermore, no studies are currently available dealing with the simultaneous measurement of complete Na -H exchanger kinetics, maximal Na -Li countertransport activity and the main variables of glucose metabolism, plasma renin and aldosterone levels, plasma and urinary electrolytes and plasma lipids, all these parameters being indirectly involved in Na -H exchanger regulation [8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Erythrocyte Na⁺–H⁺ exchanger kinetics and Na⁺–Li⁺ countertransport activity in essential hypertensive patients

Delva¹,

Pastori²,

Degan³

et al. 1996

Eur J Clin Investigation

Self Cite

View full text Add to dashboard Cite

The authors measured Na(+)-H+ exchanger kinetics together with Na(+)-Li+ countertransport V(max) in the erythrocytes of 21 subjects with essential hypertension and 16 normotensive control subjects. Na(+)-H+ exchange V(max) appeared to be increased in patients with essential hypertension, while the Na(+)-H+ exchanger affinity for intracellular proton sites (K50%) proved to be unchanged and the index of cooperativity among intracellular proton binding sites as measured by Hill's coefficient (Hill's n) decreased as compared with normotensive control subjects. Na(+)-Li+ countertransport V(max) appeared to be higher in patients with essential hypertension than in control subjects. The authors were unable to find any correlations between Na(+)-H+ exchanger kinetic parameters and metabolic variables such as parameters of insulin resistance and plasma lipids. On the basis of the data obtained, erythrocyte Na(+)-H+ exchanger activity was found to be abnormal in two kinetic variables in essential hypertensive patients and showed no simple linear correlations with the main variables of glucose metabolism, plasma lipids, renin or aldosterone.

show abstract

Erythrocyte Na⁺‐H⁺ exchanger and Na⁺‐Li⁺ countertransport activity in primary aldosteronism

Cited by 9 publications

References 15 publications

Sgk1 Sensitive Pendrin Expression in Murine Platelets

Sgk1 Sensitive Pendrin Expression in Murine Platelets

The Li sup sup Na sup nbsp sup exchange in hypertension

Erythrocyte Na⁺–H⁺ exchanger kinetics and Na⁺–Li⁺ countertransport activity in essential hypertensive patients

Contact Info

Product

Resources

About

Erythrocyte Na+‐H+ exchanger and Na+‐Li+ countertransport activity in primary aldosteronism

Cited by 9 publications

References 15 publications

Sgk1 Sensitive Pendrin Expression in Murine Platelets

Sgk1 Sensitive Pendrin Expression in Murine Platelets

The Li sup sup Na sup nbsp sup exchange in hypertension

Erythrocyte Na+–H+ exchanger kinetics and Na+–Li+ countertransport activity in essential hypertensive patients

Contact Info

Product

Resources

About

Erythrocyte Na⁺‐H⁺ exchanger and Na⁺‐Li⁺ countertransport activity in primary aldosteronism

Erythrocyte Na⁺–H⁺ exchanger kinetics and Na⁺–Li⁺ countertransport activity in essential hypertensive patients