Molecular mechanisms of sodium transport inhibition in proximal tubule during acute hypertension

Current Opinion in Nephrology and Hypertension

Volumn 9, Issue 2, 2000, Pages 149-156

  Magyar, Clara E ^a   McDonough, Alicia A ^a  

^a UNIVERSITY OF SOUTHERN CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ADENOSINE TRIPHOSPHATASE (POTASSIUM SODIUM); PARATHYROID HORMONE; SODIUM;

AUTOREGULATION; GLOMERULUS FILTRATION RATE; HUMAN; HYPERTENSION; KIDNEY BLOOD FLOW; KIDNEY PROXIMAL TUBULE; MACULA DENSA; NATRIURESIS; PRIORITY JOURNAL; REVIEW; SIGNAL TRANSDUCTION; SODIUM TRANSPORT; WATER ABSORPTION;

ACUTE DISEASE; BASEMENT MEMBRANE; CARRIER PROTEINS; CHRONIC DISEASE; HUMANS; HYPERTENSION, RENAL; KIDNEY TUBULES, PROXIMAL; NA(+)-K(+)-EXCHANGING ATPASE; SODIUM; SODIUM-HYDROGEN ANTIPORTER; SODIUM-PHOSPHATE COTRANSPORTER PROTEINS; SYMPORTERS;

EID: 0034011585     PISSN: 10624821     EISSN: None     Source Type: Journal    
DOI: 10.1097/00041552-200003000-00009     Document Type: Review

References (41)

1. 1 Cowley AW, Roman RJ. The role of the kidney in hypertension. JAMA 1996; 275:1581-1589.
2. 2 Chou C-L, Marsh DJ. Role of proximal convoluted tubule in pressure diuresis in the rat. Am J Physiol 1986; 251:F283-289.
3. 3 Chou C-L, Marsh DJ. Time course of proximal tubule response to acute hypertension in the rat. Am J Physiol 1988; 254:F601-607.
4. 4 Kinoshita Y, Knox FG. Response of superficial proximal convoluted tubules to decreased and increased renal perfusion pressure. Circ Res 1990; 66:1184-1189.
5. 5 Schnermann J, Briggs JP. The macula densa is worth its salt. J Clin Invest 1999; 104:1007-1009. A succinct and timely commentary on TGF with a focus on how and why TGF is reset during various challenges.
6. 6 Lorenz JN, Schultheis PJ, Traynor T, Shull GE, Schnermann J. Micropuncture analysis of single-nephron function in NHE3-deficient mice. Am J Physiol 1999; 277:F447-F453. The results of this study demonstrate that NHE3 is a major sodium transport route in the PT, and the impact of reducing sodium reabsorption on TGF and loop reabsorption.
7. 7 Hensley CB, Bradley ME, Mircheff AK. Parathyroid hormone induced translocation of Na-H antiporters in rat proximal tubules. Am J Physiol 1989; 257:C637-C645.
8. 8 Lotscher M, Kaissling B, Biber J, Murer H, Levi M. Role of microtubules in the rapid regulation of renal phosphate transport in response to acute alterations in dietary phosphate content. J Clin Invest 1997; 99:1302-1312.
9. 9 Biemesderfer D, Rutherford PA, Nagy T, Pizzonia JH, Abu-Alfa A, Aronson PS. Monoclonal antibodies for high resolution localization of NHE-3 in adult and neonatal rat kidney. Am J Physiol 1997; 273:F289-299.
10. 10 Chibalin AV, Ogimoto G, Pedemonte CH, Pressley TA, Katz AI, Feraille E, et al. Dopamine-induced endocytosis of Na+,K+-ATPase is initiated by phosphorylation of Ser-18 in the rat alpha subunit and is responsible for the decreased activity in epithelial cells. J Biol Chem 1999; 274:1920-1927. A very careful study that analyzes the molecular mechanisms responsible for depressed Na-K-ATPase-mediated transport during dopamine stimulation. The activity and trafficking regulation of sodium pump alpha subunit are analyzed in parallel. The paper addresses the controversial issue of the role of phosphorylation of two serines found in the N-terminal region, and concludes that phosphorylation of one, not the other, mediates internalization, and that ATPase activity was unaffected by phosphorylation of either site.
11. 2. Am J Physiol 1997; 272:F781-788.
12. 12 Leyssac PP, Christensen P. A comparison between endogenous and exogenous lithium clearance in the anesthetized rat. Acta Physiol Scand 1994; 151:173-179.
13. 13 Zhang YB, Mircheft AK, Magyar CE, Warnock DG, Hensley CB, Yip K-P, et al. Rapid redistribution and inhibition of sodium transporters during natriuresis induced by acute hypertension. Am J Physiol 1996; 270:F1004-1014.
14. 14 Zhang Y, Magyar CE, Norian JM, Holstein-Rathlou N-H, Mircheff AK, McDonough AA. Reversible effects of acute hypertension on proximal tubule sodium transporters. Am J Physiol 1998; 274:C1090-C1100. This study extends the initial observation that acute hypertension depresses PT sodium transport by internalization of NHE3 and inhibition of Na-K-ATPase. It demonstrates that the responses are acutely reversible, that there is trafficking of NaPi as well as NHE3, and fails to detect internalization of Na-K-ATPase during acute hypertension.
15. 15 Yip K-P, Tse C-M, McDonough AA, Marsh DJ. Redistribution of Na/H exchanger isoform NHE3 in proximal tubules induced by acute and chronic hypertension. Am J Physiol 1998; 275:F565-F575. This study extends the initial observation that acute hypertension depresses PT sodium transport by internalization of NHE3 (obtained by subcellular fractionation) by providing immunocytochemical evidence for the redistribution of NHE3 to the base of the brush border co-localized with clathrin-coated pits.
16. 16 Zhang YB, Magyar CE, Holstein-Rathlou N-H, McDonough AA. The cytochrome P450 inhibitor cobalt chloride prevents inhibition of renal Na,K-ATPase and redistribution of apical NHE-3 during acute hypertension. J Am Soc Nephrol 1998; 9:531-537. The first report to dissect the signalling responsible for the depressed PT sodium transport during acute hypertension. Although cobalt treatment did not change blood pressure or V, it did blunt the responses to acute hypertension at the whole kidney and molecular levels.
17. 17 Zhang Y, Norian JM, Magyar CE, Holstein-Rathlou N-H, Mircheff AK, McDonough AA. In vivo PTH provokes apical NHE3 and NaPi2 redistriubtion and Na-K-ATPase inhibition. Am J Physiol 1999; 276:F711-F719. One of the two initial papers, both published last year, that defines the molecular mechanisms responsible for depressed PT sodium transport during PTH treatment in vivo. Responses are strikingly similar to those seen with acute hypertension: internalization of apical NHE3 and NaPi and inhibition of Na-K-ATPase. It also dissects the signalling responsible for the responses by using PTH analogue, which does not stimulate AC.
18. 18 Fan L, Wiederkehr MR, Collazo R, Wang H, Crowder LA, Moe OW. Dual mechanisms of regulation of Na/H exchanger NHE-3 by parathyroid hormone in rat kidney. J Biol Chem 1999; 274:11289-11295. One of the two initial papers, both published last year, which defines the molecular mechanisms responsible for depressed PT sodium transport during PTH treatment in vivo. This report focuses on apical NHE3 and provides evidence that there is a rapid decrease in NHE3 activity followed by a microtubular-dependent removal from the brush border.
19. 19 Lotscher M, Scarpetta Y, Levi M, Halaihel N, Wang H, Zajicek HK, et al. Rapid downregulation of rat renal Na/Pi cotransporter in response to parathyroid hormone involves microtubule rearrangement. J Clin Invest 1999; 104:483-494. This group was the first to demonstrate that microtubule-specrfic drugs could be used in the whole animal in vivo to analyze the role of microtubules in the trafficking of transporters. Using confocal microscopy, the paper very elegantly details the effects of the drugs on the spatial organization of the microtubules, as well as analyzes NaPi distribution biochemically and using microscopy.
20. 20 Biemesderfer D, Nagy T, DeGray B, Aronson PS. Specific association of megalin and the Na/H exchanger isoform NHE3 in the proximal tubule. J Biol Chem 1999; 274:17518-17524. This report is especially significant as NHE3 redistributes to the intermicrovillar cleft region in response to acute hypertension, suggesting that the association may play a role in the internalization of NHE3 during acute hypertension or PTH treatment.
21. 21 Moe O. Acute regulation of proximal tubule apical membrane Na/H exchanger NHE3: role of phosphorylation, protein trafficking and regulatory factors. J Am Soc Nephrol 1999; 10:2412-2425. Dr Moe is to be complimented for assembling a wide array of topics concerning NHE3 regulation into a very readable and informative review.
22. 22 Zizak M, Lamprecht G, Steplock D, Tariq N, Shenolikar S, Donowitz M, et al. cAMP-induced phosphorylation and inhibition of Na(+)/H(+) exchanger 3 (NHE3) are dependent on the presence but not the phosphorylation of NHE regulatory factor. J Biol Chem 1999; 274:24753-24758. One of the latest papers detailing the importance and mechanisms of the NHE regulatory factor in NHE3 transport regulation, all in vitro.
23. 23 Yun CH, Lamprecht G, Forster DV, Sidor A. NHE3 kinase A regulatory protein E3KARP binds the epithelial brush border Na+/H+ exchanger NHE3 and the cytoskeletal protein ezrin. J Biol Chem 1998; 273:25856-25863. This is one of two papers that provide evidence for the testable idea that the NHE3 regulatory factor E3KARP plays a critical role in bringing ezrin and PKA spatially close to NHE3, where it will phosphorylate the cytoplasmic domain when cAMP is elevated.
24. 24 Lamprecht G, Weinman EJ, Yun CH. The role of NHERF and E3KARP in the cAMP-mediated inhibition of NHE3. J Biol Chem 1998; 273:29972-22998. This is one of two papers that provide evidence for the testable idea that the NHE3 regulatory factor plays a critical role in bringing ezrin and PKA spatially close to NHE3, where it will phosphorylate the cytoplasmic domain when cAMP is elevated.
25. 25 Kurashima K, D'Souza S, Szaszi K, Ramjeesingh R, Orlowski J, Grinstein S. The apical Na(+)/H(+) exchanger isoform NHE3 is regulated by the actin cytoskeleton. J Biol Chem 1999; 274:29843-29849. This in-vitro study of transfected NHE3 suggests a functional role of actin in association with NHE3 in its recycling to and from the cell surface.
26. 26 Kurashima K, Szabo EZ, Lukacs G, Orlowski J, Grinstein S. Endosomal recycling of the Na+/H+ exchanger NHE3 isoform is regulated by the phosphatidylinositol 3-kinase pathway. J Biol Chem 1998; 273:20828-20836. This in-vitro study demonstrates that phosphatidylinositol 3-kinase regulates the endosomal recycling of NHE3 transfected into NHE3-deficient Chinese hamster ovary cells.
27. 27 Efendiev R, Bertorello AM, Pedemonte CH. PKC-beta and PKC-zeta mediate opposing effects on proximal tubule Na+,K+-ATPase activity. FEBS Lett 1999; 456:45-48. The puzzling and contrasting effects of PKC inhibition of Na-K-ATPase activity versus phorbol myristate acetate stimulation of Na-K-ATPase activity are addressed in this report.
28. 28 Garg LC, Narang N, McArdle S. Na,K-ATPase in nephron segments of rats developing spontaneous hypertension. Am J Physiol 1985; 249:F863-F869.
29. 29 Garg LC, Narang N. Sodium-potassium-adenosine triphosphatase in nephron segments of spontaneously hypertensive rats. J Lab Clin Med, 1985; 106:43-46.
30. 30 Hayashi M, Yoshida T, Monkawa T, Yamaji Y, Sato S, Saruta T. Na/H-exchanger 3 activity and its gene in the spontaneously hypertensive rat kidney. J Hypertens 1997; 15:43-48.
31. 31 Morduchowicz GA, Sheikh-Hamad D, Jo OD, Nord EP, Lee DB, Yanagawa N. Increased Na/H antiport activity in the renal brush border membrane of SHR. Kidney Int 1989; 365:57-581.
32. 32 Schnermann J, Traynor T, Yang T, Arend L, Huang YG, Smart A, Briggs JP. Tubuloglomerular feedback: new concepts and developments. Kidney Int 1998; 54:S40-S45. This study integrates the findings from transgenic mice that lack the angiotensin-converting enzyme gene, ATI receptor or lack nitric oxide synthase into an understanding of TGF.
33. 33 Bharatula M, Hussain T, Lokhandwala MF. Angiotensin II AT1 receptor/ signaling mechanisms in the biphasic effect of the peptide on proximal tubular Na+,K+-ATPase. Clin Exp Hypertens 1998; 20:465-480. This study addresses signalling pathways responsible for angiotensin II stimulation at low concentrations versus high concentrations to explain biphasic regulation of Na-K-ATPase activity and sodium transport.
34. 34 Leyssac PP, Karlsen FM, Holstein-Rathlou NH. Effect of angiotensin II receptor blockade on proximal tubular fluid reabsorption. Am J Physiol 1997; 273:R510-R517.
35. 35 Mannstadt M, Juppner H, Gardella TJ. Receptors for PTH and PTHrP: their biological importance and functional properties. Am J Physiol 1999; 277:F665-F675. A valuable updated mini-handbook for PTH, PTHrP research.
36. 36 Maeda S, Sutliff RL, Qian J, Lorenz JN, Wang J, Tang H, et al. Targeted overexpression of parathyroid hormone-related protein (PTHrP) to vascular smooth muscle in transgenic mice lowers blood pressure and alters vascular contractility. Endocrinology 1999; 140:1815-1825. This study establishes the importance of PTHrP as a regulator of blood pressure.
37. 37 Qian J, Lorenz JN, Maeda S, Sutliff RL, Weber C, Nakayama T, et al. Reduced blood pressure and increased sensitivity of the vasculature to parathyroid hormone-related protein (PTHrP) in transgenic mice overexpressing the PTH/ PTHrP receptor in vascular smooth muscle. Endocrinology 1999; 140:1826-1833. This study establishes the PTH/PTHrP system as one that regulates blood pressure.
38. 38 Crass MF, Scarpace PJ. Vasoactive properties of a parathyroid hormone-related protein in the rat aorta. Peptides 1993; 14:179-183.
39. 39 Noda M, Katoh T, Kurokawa K, Takuwa Y. Increased expression of parathyroid hormone-related peptide gene in blood vessels of spontaneously hypertensive rats. Hypertension 1997; 30:1284-1288.
40. 40 Hussain T, Lokhandwala MF. Renal dopamine receptor function in hypertension. Hypertension 1998; 32:187-197. An insightful and provocative review of the somewhat complicated field of dopamine and blood pressure.
41. 41 Sanada H, Jose PA, Hazen-Martin D, Yu PY, Xu J, Bruns DE, et al. Dopamine-1 receptor coupling defect in renal proximal tubule cells in hypertension. Hypertension 1999; 33:1036-1042. These investigators went to the trouble to make cultured renal cell lines from humans with and without hypertension to determine whether the lesions in dopamine regulation previously characterized in rodent models were applicable to human hypertension.