Increased Na+/H+ antiport activity in the renal brush border membrane of SHR

Morduchowicz, G.; Sheikh-Hamad, David; Jo, Oak D.; Nord, Edward P.; Lee, David B. N.; Yanagawa, Norimoto

doi:10.1038/ki.1989.233

Cited by 84 publications

(43 citation statements)

References 23 publications

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“…Compared with proximal tubules from WKY rats, there was increased NHE3 activity in tubules from SHR. These findings are compatible with previous results; Morduchowicz et al, 1989;Dagher and Sauterey, 1992;Hayashi et al, 1997). Furthermore, we showed that the sensitivity of the enhanced NHE3 activity in proximal tubules was about 50-fold higher in SHR compared with WKY rats.…”

Section: Discussionsupporting

confidence: 83%

“…22 Na uptake studies were performed according to Morduchowicz et al (1989). In brief, purified BBMV were prepared by Mg 2ϩ precipitation method from SHR and WKY treated with Y-27632 or vehicle in vivo.…”

Section: Methodsmentioning

confidence: 99%

“…Protein concentration was measured by Coomassie brilliant blue with bovine serum albumin as the reference protein. The initial 22 Na uptake rate was expressed in moles per milligram protein per 5 s (Morduchowicz et al, 1989).…”

Section: Methodsmentioning

confidence: 99%

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Inhibition of Rho-Kinase Reduces Renal Na-H Exchanger Activity and Causes Natriuresis in Rat

Nishiki

Tsuruoka²,

Kawaguchi³

et al. 2003

J Pharmacol Exp Ther

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Rho-kinase regulates the actin cytoskeleton and therefore modulates transport. The role of Rho-kinase in Na-H exchanger (NHE) activity of rat proximal convoluted tubules (PCTs) was investigated using (R)-(ϩ)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide (Y-27632), a specific inhibitor of Rho-kinase. In spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats, apical and basolateral NHE activities were determined by measuring cell pH recovery following luminal NH 4 ϩ prepulse and basolateral sodium removal, respectively. Apical NHE activity was greater in 8 to 9 week old hypertensive SHR compared with WKY. Although Y-27632 suppressed pH i recovery in both strains, sensitivity was 50-fold higher in adult SHR. Y-27632 suppressed basolateral NHE in both strains with similar sensitivity. Apical NHE activity was not greater in 5-week-old, not yet hypertensive, SHR rats compared with WKY. In clearance studies, Na excretion was less in SHR than in WKY rats. Y-27632 increased Na excretion and fractional excretion Na in both strains but more so in SHR.22 Na uptake of the brush border membrane vesicle taken from Y-27632-treated rats decreased more than that from vehicletreated animals in both adult SHR and WKY. We conclude that apical NHE activity is increased in SHR PCT compared with controls and that inhibition of Rho-kinase reduces PCT NHE activities and causes natriuresis.

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Section: Discussionsupporting

confidence: 83%

Section: Methodsmentioning

confidence: 99%

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Inhibition of Rho-Kinase Reduces Renal Na-H Exchanger Activity and Causes Natriuresis in Rat

Nishiki

Tsuruoka²,

Kawaguchi³

et al. 2003

J Pharmacol Exp Ther

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“…Furthermore, nifedipine consistently elevated intracellular pH values (23). An enhanced activity of the H + -Na + antiporter (as a major mechanism of cell defense against cellular acidification) has been reported in lymphocytes (24) as well as in the renal brush border membrane of spontaneously hypertensive rats (25) and in hypertensive rats (26). Other authors have shown enhanced responsiveness of the renal proximal Na + -H + antiporter of hypertensive rats to stimulation with some hormones (27).…”

Section: Discussionmentioning

confidence: 86%

Catecholamine-induced vasoconstriction is sensitive to carbonic anhydrase I activation

Puşcaş¹,

Coltâu²,

Gilau³

et al. 2001

Braz J Med Biol Res

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We studied the relationship between alpha-and beta-adrenergic agonists and the activity of carbonic anhydrase I and II in erythrocyte, clinical and vessel studies. Kinetic studies were performed. Adrenergic agonists increased erythrocyte carbonic anhydrase as follows: adrenaline by 75%, noradrenaline by 68%, isoprenaline by 55%, and orciprenaline by 62%. The kinetic data indicated a non-competitive mechanism of action. In clinical studies carbonic anhydrase I from erythrocytes increased by 87% after noradrenaline administration, by 71% after orciprenaline and by 82% after isoprenaline. The increase in carbonic anhydrase I paralleled the increase in blood pressure. Similar results were obtained in vessel studies on piglet vascular smooth muscle. We believe that adrenergic agonists may have a dual mechanism of action: the first one consists of a catecholamine action on its receptor with the formation of a stimulus-receptor complex. The second mechanism proposed completes the first one. By this second component of the mechanism, the same stimulus directly acts on the carbonic anhydrase I isozyme (that might be functionally coupled with adrenergic receptors), so that its activation ensures an adequate pH for stimulus-receptor coupling for signal transduction into the cell, resulting in vasoconstriction. Correspondence

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“…This enhanced responsiveness in SHR kidney may be partially explained by α 2B -adrenoceptor-mediated acceleration of Na + /H + exchange. The latter may be explained by an increased activity of the Na + /H + exchanger (NHE) in the kidney of the hypertensive rat strains, namely the SHR (44,45) that is unresponsive to inhibitory action (46). This increased expression of NHE in the kidney of SHR compared to WKY rats (47) has been related to the development of hypertension in these animals (48).…”

Section: Discussionmentioning

confidence: 99%

Effect of Clonidine on Renal Sodium Handling in Spontaneously Hypertensive Rats

Vieira-Coelho

Moura

2012

J Pharmacol Sci

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Abstract. Up-regulation of kidney α 2 -adrenoceptor expression has been implicated in the development of hypertension in spontaneously hypertensive rats (SHR). This study was carried out to evaluate renal sodium excretion in response to clonidine administration in SHR and control normotensive Wistar-Kyoto (WKY) rats. SHR and WKY rats (12-week-old) were placed in metabolic cages for 4 days: the first 2 days in control conditions and the following 2 days under oral clonidine treatment (100 μg/kg body weight). Clonidine produced a similar reduction in systolic blood pressure values in SHR and WKY rats, although SHR remained hypertensive. At the end of the study SHR and WKY rats presented similar noradrenaline plasma levels. However, noradrenaline kidney tissue levels were significantly higher in SHR compared to WKY rats. Under control conditions, SHR presented lower urine flow compared to WKY rats. Clonidine produced a significant decrease in urine flow in WKY rats but not in SHR. Furthermore, clonidine also produced a significant reduction in urinary sodium, potassium, and creatinine excretion in WKY rats, but had no effect in SHR. In conclusion, in SHR the reduction in systolic blood pressure and sympathetic activity produced by clonidine was not accompanied by a decrease in urine volume and sodium excretion.

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Increased Na+/H+ antiport activity in the renal brush border membrane of SHR

Cited by 84 publications

References 23 publications

Inhibition of Rho-Kinase Reduces Renal Na-H Exchanger Activity and Causes Natriuresis in Rat

Inhibition of Rho-Kinase Reduces Renal Na-H Exchanger Activity and Causes Natriuresis in Rat

Catecholamine-induced vasoconstriction is sensitive to carbonic anhydrase I activation

Effect of Clonidine on Renal Sodium Handling in Spontaneously Hypertensive Rats

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