nach oben

Current Hypertension Reports

Erschienen in:

01.04.2010

Modulation of Pressure-Natriuresis by Renal Medullary Reactive Oxygen Species and Nitric Oxide

verfasst von: Paul M. O’Connor, Allen W. Cowley Jr.

Erschienen in: Current Hypertension Reports | Ausgabe 2/2010

Einloggen, um Zugang zu erhalten

Abstract

The renal pressure-natriuresis mechanism is the dominant controller of body fluid balance and long-term arterial pressure. In recent years, it has become clear that the balance of reactive oxygen and nitrogen species within the renal medullary region is a key determinant of the set point of the renal pressure-natriuresis curve. The development of renal medullary oxidative stress causes dysfunction of the pressure-natriuresis mechanism and contributes to the development of hypertension in numerous disease models. The purpose of this review is to point out the known mechanisms within the renal medulla through which reactive oxygen and nitrogen species modulate the pressure-natriuresis response and to update the reader on recent advances in this field.

Guyton AC: Dominant role of the kidneys and accessory role of whole-body autoregulation in the pathogenesis of hypertension. Am J Hypertens 1989, 2(7):575–585.PubMed

Cowley AW Jr, Mattson DL, Lu S, Roman RJ: The renal medulla and hypertension. Hypertension 1995, 25(4 Pt 2):663–673.PubMed

Cowley AW Jr: Renal medullary oxidative stress, pressure-natriuresis, and hypertension. Hypertension 2008, 52(5):777–786.CrossRefPubMed

Evans RG, Majid DS, Eppel GA: Mechanisms mediating pressure natriuresis: what we know and what we need to find out. Clin Exp Pharmacol Physiol 2005, 32(5–6):400–409.CrossRefPubMed

Cowley AW, Roman RJ, Fenoy FJ, Mattson DL: Effect of renal medullary circulation on arterial pressure. J Hypertens Suppl 1992, 10(7):S187–S193.CrossRefPubMed

Garcia-Estan J, Roman RJ: Role of renal interstitial hydrostatic pressure in the pressure diuresis response. Am J Physiol 1989, 256(1 Pt 2):F63–F70.PubMed

Williams JM, Sarkis A, Lopez B, et al.: Elevations in renal interstitial hydrostatic pressure and 20-hydroxyeicosatetraenoic acid contribute to pressure natriuresis. Hypertension 2007, 49(3):687–694.CrossRefPubMed

Zhang YB, Magyar CE, Holstein-Rathlou NH, McDonough AA: The cytochrome P-450 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(4):531–537.PubMed

Cowley AW Jr: Long-term control of arterial blood pressure. Physiol Rev 1992, 72(1):231–300.PubMed

10.

Majid DS, Navar LG: Nitric oxide in the mediation of pressure natriuresis. Clin Exp Pharmacol Physiol 1997, 24(8):595–599.CrossRefPubMed

11.

Guarasci GR, Kline RL: Pressure natriuresis following acute and chronic inhibition of nitric oxide synthase in rats. Am J Physiol 1996, 270(2 Pt 2):R469–R478.PubMed

12.

Mattson DL, Roman RJ, Cowley AW Jr: Role of nitric oxide in renal papillary blood flow and sodium excretion. Hypertension 1992, 19(6 Pt 2):766–769.PubMed

13.

Mattson DL, Lu S, Nakanishi K, et al.: Effect of chronic renal medullary nitric oxide inhibition on blood pressure. Am J Physiol 1994, 266(5 Pt 2):H1918–H1926.PubMed

14.

Szentivanyi M Jr, Zou AP, Mattson DL, et al.: Renal medullary nitric oxide deficit of Dahl S rats enhances hypertensive actions of angiotensin II. Am J Physiol Regul Integr Comp Physiol 2002, 283(1):R266–R272.PubMed

15.

O’Connor PM, Cowley AW Jr: Vasopressin-induced nitric oxide production in rat inner medullary collecting duct is dependent on V2 receptor activation of the phosphoinositide pathway. Am J Physiol Renal Physiol 2007, 293(2):F526–532.CrossRefPubMed

16.

Szentivanyi M Jr, Maeda CY, Cowley AW Jr: Local renal medullary L-NAME infusion enhances the effect of long-term angiotensin II treatment. Hypertension 1999, 33(1 Pt 2):440–445.PubMed

17.

Park F, Zou AP, Cowley AW Jr: Arginine vasopressin-mediated stimulation of nitric oxide within the rat renal medulla. Hypertension 1998, 32(5):896–901.PubMed

18.

Yuan B, Cowley AW Jr: Evidence that reduced renal medullary nitric oxide synthase activity of dahl s rats enables small elevations of arginine vasopressin to produce sustained hypertension. Hypertension 2001, 37(2 Part 2):524–528.

19.

Fenoy FJ, Ferrer P, Carbonell L, Garcia-Salom M: Role of nitric oxide on papillary blood flow and pressure natriuresis. Hypertension 1995, 25(3):408–414.PubMed

20.

•• Jin C, Hu C, Polichnowski A, et al.: Effects of renal perfusion pressure on renal medullary hydrogen peroxide and nitric oxide production. Hypertension 2009, 53(6):1048–1053. Using in vivo microdialysis techniques, Jin et al. demonstrate that increasing renal perfusion pressure stimulates renal medullary NO and H ₂ O ₂ . Importantly, NO stimulation was not affected by renal decapsulation and inhibition of the renal natriuretic response, suggesting that the increased production of NO may be a primary event in the renal pressure-natriuresis cascade.

21.

Ortiz PA, Hong NJ, Garvin JL: NO decreases thick ascending limb chloride absorption by reducing Na(+)-K(+)-2Cl(-) cotransporter activity. Am J Physiol Renal Physiol 2001, 281(5):F819–F825.PubMed

22.

• Lieb DC, Kemp BA, Howell NL, et al.: Reinforcing feedback loop of renal cyclic guanosine 3′5′-monophosphate and interstitial hydrostatic pressure in pressure-natriuresis. Hypertension 2009, 54(6):1278–1283. Lieb et al. demonstrate that cyclic guanosine 3′5′-monophosphate is produced in response to increases in RIHP and also acts to increase RIHP through an unknown mechanism. By activating a positive feedback loop, cyclic guanosine 3′5′-monophosphate may allow the kidney to rapidly reduce sodium and water reabsorption when renal perfusion pressure is elevated.

23.

Wu F, Park F, Cowley AW Jr, Mattson DL: Quantification of nitric oxide synthase activity in microdissected segments of the rat kidney. Am J Physiol 1999, 276(6 Pt 2):F874–F881.PubMed

24.

Zhang Z, Pallone TL: Response of descending vasa recta to luminal pressure. Am J Physiol Renal Physiol 2004, 287(3):F535–F542.CrossRefPubMed

25.

•• Schneider MP, Ge Y, Pollock DM, et al.: Collecting duct-derived endothelin regulates arterial pressure and Na excretion via nitric oxide. Hypertension 2008, 51(6):1605–1610. Schneider et al. demonstrate that that mice lacking collecting-duct endothelin display elevated blood pressure and an altered pressure-natriuresis response, indicating that this pathway contributes to long-term blood pressure control.

26.

Nakano D, Pollock JS, Pollock DM: Renal medullary ETB receptors produce diuresis and natriuresis via NOS1. Am J Physiol Renal Physiol 2008, 294(5):F1205–F1211.CrossRefPubMed

27.

Abe M, O’Connor P, Kaldunski M, et al.: Effect of sodium delivery on superoxide and nitric oxide in the medullary thick ascending limb. Am J Physiol Renal Physiol 2006, 291(2):F350–F357.CrossRefPubMed

28.

Hong NJ, Garvin JL: Flow increases superoxide production by NADPH oxidase via activation of Na-K-2Cl cotransport and mechanical stress in thick ascending limbs. Am J Physiol Renal Physiol 2007, 292(3):F993–F998.CrossRefPubMed

29.

Makino A, Skelton MM, Zou AP, et al.: Increased renal medullary oxidative stress produces hypertension. Hypertension 2002, 39(2 Pt 2):667–672.CrossRefPubMed

30.

Taylor NE, Cowley AW Jr: Effect of renal medullary H2O2 on salt-induced hypertension and renal injury. Am J Physiol Regul Integr Comp Physiol 2005, 289(6):R1573–R1579.PubMed

31.

Chen YF, Cowley AW Jr, Zou AP: Increased H(2)O(2) counteracts the vasodilator and natriuretic effects of superoxide dismutation by tempol in renal medulla. Am J Physiol Regul Integr Comp Physiol 2003, 285(4):R827–R833.PubMed

32.

Mori T, O’Connor PM, Abe M, Cowley AW Jr: Enhanced superoxide production in renal outer medulla of Dahl salt-sensitive rats reduces nitric oxide tubular-vascular cross-talk. Hypertension 2007, 49(6):1336–1341.CrossRefPubMed

33.

•• Hong NJ, Garvin JL: Nitric oxide reduces flow-induced superoxide production via cGMP-dependent protein kinase in thick ascending limbs. Am J Physiol Renal Physiol 2009, 296(5):F1061–F1066. Hong et al. demonstrate that most of the reduction of O ₂ ⁻ levels in medullary thick ascending limb in response to increased NO produced by luminal flow occurs via the activation of cellular cGMP and protein kinase G (PKG), not direct scavenging of O ₂ ⁻ by NO to form OONO ⁻.

34.

Muzaffar S, Shukla N, Bond M, et al.: Acute inhibition of superoxide formation and Rac1 activation by nitric oxide and iloprost in human vascular smooth muscle cells in response to the thromboxane A2 analogue, U46619. Prostaglandins Leukot Essent Fatty Acids 2008, 78(4–5):247–255.CrossRefPubMed

35.

Juncos R, Garvin JL: Superoxide enhances Na-K-2Cl cotransporter activity in the thick ascending limb. Am J Physiol Renal Physiol 2005, 288(5):F982–F987.CrossRefPubMed

36.

Juncos R, Hong NJ, Garvin JL: Differential effects of superoxide on luminal and basolateral Na+/H + exchange in the thick ascending limb. Am J Physiol Regul Integr Comp Physiol 2006, 290(1):R79–R83.PubMed

37.

Taylor NE, Glocka P, Liang M, Cowley AW Jr: NADPH oxidase in the renal medulla causes oxidative stress and contributes to salt-sensitive hypertension in Dahl S rats. Hypertension 2006, 47(4):692–698.CrossRefPubMed

38.

Garcia NH, Plato CF, Stoos BA, Garvin JL: Nitric oxide-induced inhibition of transport by thick ascending limbs from Dahl salt-sensitive rats. Hypertension 1999, 34(3):508–513.PubMed

39.

Riazi S, Tiwari S, Sharma N, et al.: Abundance of the Na-K-2Cl cotransporter NKCC2 is increased by high-fat feeding in Fischer 344 X Brown Norway (F1) rats. Am J Physiol Renal Physiol 2009, 296(4):F762–F770.CrossRefPubMed

40.

Kurtz TW: Genetic models of hypertension. Lancet 1994, 344(8916):167–168.CrossRefPubMed

41.

Li N, Yi FX, Spurrier JL, et al.: Production of superoxide through NADH oxidase in thick ascending limb of Henle’s loop in rat kidney. Am J Physiol Renal Physiol 2002, 282(6):F1111–F1119.PubMed

42.

• O’Connor PM, Lu L, Schreck C, Cowley AW Jr: Enhanced amiloride-sensitive superoxide production in renal medullary thick ascending limb of Dahl salt-sensitive rats. Am J Physiol Renal Physiol 2008, 295(3):F726–F733. The authors demonstrate that O ₂ ⁻ production is enhanced in medullary thick ascending limb from Dahl salt-sensitive rats and that this enhanced O ₂ ⁻ production is sensitive to inhibition by amiloride analogues.

43.

•• O’Connor PM, Lu L, Liang M, Cowley AW Jr: A novel amiloride-sensitive H⁺ transport pathway mediates enhanced superoxide production in thick ascending limb of salt-sensitive rats, not Na⁺/H⁺ exchange. Hypertension 2009, 54(2):248–254. In this follow-up study, the authors demonstrate that excess amiloride-sensitive O ₂ ⁻ production observed in medullary thick ascending limb of Dahl salt-sensitive rats is related to activation of a novel H ⁺ transport pathway, a pathway that is upregulated in the Dahl salt-sensitive rat.

44.

O’Connor PM: Renal oxygen delivery: matching delivery to metabolic demand. Clin Exp Pharmacol Physiol 2006, 33(10):961–967.CrossRefPubMed

45.

Herrera M, Ortiz PA, Garvin JL: Regulation of thick ascending limb transport: role of nitric oxide. Am J Physiol Renal Physiol 2006, 290(6):F1279–F1284.CrossRefPubMed

46.

Brown GC: Nitric oxide regulates mitochondrial respiration and cell functions by inhibiting cytochrome oxidase. FEBS Lett 1995, 369(2–3):136–139.CrossRefPubMed

47.

Welch WJ: Intrarenal oxygen and hypertension. Clin Exp Pharmacol Physiol 2006, 33(10):1002–1005.CrossRefPubMed

48.

Welch WJ, Blau J, Xie H, et al.: Angiotensin-induced defects in renal oxygenation: role of oxidative stress. Am J Physiol Heart Circ Physiol 2005, 288(1):H22–H28.CrossRefPubMed

49.

Chen Y, Gill PS, Welch WJ: Oxygen availability limits renal NADPH-dependent superoxide production. Am J Physiol Renal Physiol 2005, 289(4):F749–F753.CrossRefPubMed

50.

•• Li N, Chen L, Yi F, et al.: Salt-sensitive hypertension induced by decoy of transcription factor hypoxia-inducible factor-1alpha in the renal medulla. Circ Res 2008, 102(9):1101–1108. Li et al. demonstrate the importance of HIF signaling in the maintenance of blood pressure in rats fed high-sodium diets. Inhibition of HIF signaling specifically in the renal medulla resulted in marked salt sensitivity of blood pressure in otherwise normotensive, salt-resistant Sprague-Dawley rats.

Titel: Modulation of Pressure-Natriuresis by Renal Medullary Reactive Oxygen Species and Nitric Oxide
verfasst von: Paul M. O’Connor
Allen W. Cowley Jr.
Publikationsdatum: 01.04.2010
Verlag: Current Science Inc.
Erschienen in: Current Hypertension Reports / Ausgabe 2/2010
Print ISSN: 1522-6417
Elektronische ISSN: 1534-3111
DOI: https://doi.org/10.1007/s11906-010-0094-6

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

^{Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag}

Kostenlos registrieren

Neu im Fachgebiet Innere Medizin

Echinokokkose medikamentös behandeln oder operieren?

06.05.2024 DCK 2024 Kongressbericht

Die Therapie von Echinokokkosen sollte immer in spezialisierten Zentren erfolgen. Eine symptomlose Echinokokkose kann – egal ob von Hunde- oder Fuchsbandwurm ausgelöst – konservativ erfolgen. Wenn eine Op. nötig ist, kann es sinnvoll sein, vorher Zysten zu leeren und zu desinfizieren.

Umsetzung der POMGAT-Leitlinie läuft

03.05.2024 DCK 2024 Kongressbericht

Seit November 2023 gibt es evidenzbasierte Empfehlungen zum perioperativen Management bei gastrointestinalen Tumoren (POMGAT) auf S3-Niveau. Vieles wird schon entsprechend der Empfehlungen durchgeführt. Wo es im Alltag noch hapert, zeigt eine Umfrage in einem Klinikverbund.

Proximale Humerusfraktur: Auch 100-Jährige operieren?

01.05.2024 DCK 2024 Kongressbericht

Mit dem demographischen Wandel versorgt auch die Chirurgie immer mehr betagte Menschen. Von Entwicklungen wie Fast-Track können auch ältere Menschen profitieren und bei proximaler Humerusfraktur können selbst manche 100-Jährige noch sicher operiert werden.

Die „Zehn Gebote“ des Endokarditis-Managements

30.04.2024 Endokarditis Leitlinie kompakt

Worauf kommt es beim Management von Personen mit infektiöser Endokarditis an? Eine Kardiologin und ein Kardiologe fassen die zehn wichtigsten Punkte der neuen ESC-Leitlinie zusammen.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen

Springer Medizin

Abstract

Bitte loggen Sie sich ein, um Zugang zu diesem Inhalt zu erhalten

Weitere Artikel der Ausgabe 2/2010

Regression of Small Resistance Artery Structural Alterations in Hypertension by Appropriate Antihypertensive Treatment

Oxidative Stress and Hypertension: Current Concepts

Carotid Baroreflex Activation: Past, Present, and Future

The Obesity Paradox and Cardiovascular Disease

Midkine Regulation of the Renin-Angiotensin System