Brain Na+,K+-ATPase isozyme activity and protein expression in ouabain-induced hypertension

Kent, Mary-Anne H.; Huang, Bing; Huysse, James W. Van; Leenen, Frans H. H.

doi:10.1016/j.brainres.2004.05.059

Cited by 12 publications

(6 citation statements)

References 40 publications

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“…Previously, we demonstrated that ouabain-induced hypertension is associated with regional changes in the activity of the ouabain-sensitive sodium pump and of the expression of the α 1 and α 2 Na + , K + -ATPase isoforms in the vascular smooth muscle (Rossoni et al, 2002). Kent et al (2004) also showed that chronic treatment with ouabain for 14 days directly inhibits Na + , K + -ATPase activity in the hypothalamus and up-regulated the α 3 isoform expression while α 1 and α 2 expression remains unchanged. Our findings reinforce those results, because in the left ventricle from ouabain-hypertensive rats there is an increment in the α 1 and α 2 isoforms of Na + , K + -ATPase.…”

Section: Discussionmentioning

confidence: 93%

Ouabain-induced hypertension enhances left ventricular contractility in rats

et al. 2006

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Section: Discussionmentioning

confidence: 93%

Ouabain-induced hypertension enhances left ventricular contractility in rats

et al. 2006

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“…Brain endogenous ouabain was found to be responsive to acute and chronic NaCl loading in Dahl salt-sensitive rats, [9][10][11]. In previous studies of the mechanisms of central effects of ouabain, doses of intracerebroventricularly administered ouabain sufficient Intrahippocampal ouabain microinjection Fedorova et al 1841 to raise the arterial pressure in rats ranged from 10 to 200 ng [29][30][31][32][33][34]. In our present experiment, a single intrahippocampal injection of a two orders of concentration lesser dose of ouabain (60 pg) produced a 40 mmHg increase in SBP, a substantial inhibition of the renal and vascular sodium pump, and a natriuretic response.…”

Section: Discussionmentioning

confidence: 96%

Intrahippocampal microinjection of an exquisitely low dose of ouabain mimics NaCl loading and stimulates a bufadienolide Na/K-ATPase inhibitor

Федорова¹,

Журавин²,

Agalakova³

et al. 2007

Journal of Hypertension

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“…3 Alternatively, CSF [Na ϩ ] may increase through other mechanisms, and the resultant increase in concentration of ouabain would also inhibit the pump but also enhance Na ϩ -K ϩ -ATPase expression in the CP through negative feedback. 35,36 In the current experimental design, any endogenous ouabain should have dissociated by Ϸ2 hours preincubation, 36 thereby exposing the uninhibited pump activity. In support of this second possibility, despite the somewhat larger inhibition of efflux by ouabain in S rats on high salt, ouabain still did not increase [Na ϩ ] i .…”

Section: Atpase-mediated Efflux In R But Not S Ratsmentioning

confidence: 99%

Sodium Transport in the Choroid Plexus and Salt-Sensitive Hypertension

et al. 2009

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Abstract-To elucidate the role of epithelial sodium channels (ENaCs) and Na ϩ -K ϩ -ATPase in Na ϩ transport by the choroid plexus, we studied ENaC expression and Na ϩ transport in the choroid plexus. Lateral ventricle choroid plexuses were obtained from young male Wistar, Dahl salt-resistant (SS.BN13), and Dahl salt-sensitive (SS/MCW) rats on a regular (0.3%) or high-(8.0%) salt diet. The effects of ENaC blocker benzamil and Na ϩ -K ϩ -ATPase blocker ouabain on sodium transport were evaluated by measuring the amounts of retained 22 Na ϩ and by evaluating intracellular [Na ϩ ] with Sodium Green fluorescence. In Wistar rats, ENaC distribution was as follows: microvilli, 10% to 30%; cytoplasm, 60% to 80%; and basolateral membrane, 5% to 10%. Benzamil (10 Ϫ8 Key Words: sodium Ⅲ choroid plexus Ⅲ ENaC Ⅲ Na ϩ -K ϩ -ATPase Ⅲ Dahl rats Ⅲ hypertension S trict regulation of [Na ϩ ] in the cerebrospinal fluid (CSF) and, thus, the central nervous system is crucial for normal functioning of neurons. An increase in CSF [Na ϩ ] by as little as 2 mmol/L can increase the firing rate of neurons. 1,2 A chronic 5-mmol/L increase in CSF [Na ϩ ] causes sympathetic hyperactivity and hypertension. 3 Such a subtle increase in CSF [Na ϩ ] might be a primary abnormality in salt-induced hypertension. CSF [Na ϩ ] increases by Յ5 mmol/L in Dahl salt-sensitive (S) rats and spontaneously hypertensive rats on a high-salt diet, and this increase appears to precede the increase in blood pressure, whereas CSF [Na ϩ ] shows minimal changes in "salt-resistant" strains, such as Wistar-Kyoto and Dahl salt-resistant (R) rats. 3,4 The epithelium of the choroid plexus (CP) is the major site for production of CSF, which is later absorbed by arachnoid granulations. 5,6 Net transport of Na ϩ between plasma and CSF is a balance of Na ϩ influx into and efflux out of the CP cells, which is accomplished by selective distribution and activity of a variety of enzymes and transporters. 7,8 An increase in CSF [Na ϩ ] in Dahl S rats on a high-salt diet may, thus, be attributed to an increased efflux of Na ϩ into the CSF, decreased reuptake of Na ϩ from the CSF, or both. However, the actual mechanisms contributing to the increase in CSF [Na ϩ ] in Dahl S rats or spontaneously hypertensive rats on a high-salt diet have not yet been studied.MA number of Na ϩ transporters mediate Na ϩ influx into the CP. On the basis of their distribution either on the apical or the basolateral surface, they contribute to the transport of Na ϩ from CSF or plasma into the CP cells along a prevailing electrochemical gradient. The Na ϩ channel blocker, amiloride, decreases Na ϩ transport into the CP and CSF. 9 -11 Blockade of the sodium hydrogen exchanger (NHE) was first thought to be responsible for this, but NHE proteins are almost undetectable in the CP of rats. 5,12 Amiloride also blocks epithelial sodium channels (ENaCs), which we reported recently to be present in the CP of rats. 13 ENaCs are members of the amiloride-sensitive Na ϩ channels with 3 subunits, ␣, ␤, and ␥, forming a ...

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Brain Na+,K+-ATPase isozyme activity and protein expression in ouabain-induced hypertension

Cited by 12 publications

References 40 publications

Ouabain-induced hypertension enhances left ventricular contractility in rats

Ouabain-induced hypertension enhances left ventricular contractility in rats

Intrahippocampal microinjection of an exquisitely low dose of ouabain mimics NaCl loading and stimulates a bufadienolide Na/K-ATPase inhibitor

Sodium Transport in the Choroid Plexus and Salt-Sensitive Hypertension

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