The DOI matches its Crossref record.
Role of renal hemodynamics and arterial pressure in aldosterone "escape".
Abstract
This study examined the importance of changes in renal hemodynamics and renal artery pressure (RAP) in allowing the kidneys to escape from the chronic sodium-retaining effects of aldosterone (Aldo). In five dogs in which RAP was permitted to increase during Aldo infusion (14 micrograms/kg/day), sodium excretion (UNaV) and fractional sodium excretion (FENa) decreased markedly on Day 1 and then returned to control on Days 2 to 4 of Aldo infusion as RAP and glomerular filtration rate (GFR) increased 15 to 19 mm Hg and 20% to 24%, respectively, and remained near these levels during 7 days of Aldo infusion. In seven dogs in which RAP was prevented from increasing with an electronically servo-controlled aortic occluder, UNaV decreased from 256 +/- 3 to 117 +/- 9 mEq/day on the first day and remained at 70 to 80 mEq/day below sodium intake for 7 days of Aldo infusion. Cumulative sodium balance and sodium iothalamate space increased 610 +/- 39 mEq and 3729 +/- 397 ml when RAP was servo-controlled, causing ascites in most of the dogs, while mean arterial pressure did not plateau but continued to rise to 59 +/- 3 mm Hg above control after 7 days of Aldo infusion. When the servo-controller was stopped and RAP was allowed to rise while Aldo infusion was continued, GFR rose to 126% to 136% of control, FENa increased markedly, UNaV increased to 579 +/- 64 mEq/day on the first day, and the dogs returned to normal sodium balance. These data indicate that an increase in RAP, which raises GFR and FENa, is essential in allowing the kidneys to escape from the chronic sodium-retaining action of Aldo and to achieve sodium balance and a stable level of arterial pressure without severe volume expansion and ascites.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“aldosterone activates MRs expressed on macula densa cells and increases their production of NO, which induces renal vasodilation and glomerular hyperfiltration48,49.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [48]
Citations
Cited by
Sorted by citations
Pickering, T. G., Hall, J. E., Appel, L. J., Falkner, B. E., Graves, J., Hill, M. N., Jones, D. W., Kurtz, T., Sheps, S. G., & Roccella, E. J. (2005) · Hypertension · doi:10.1161/01.hyp.0000150859.47929.8e · Cited by 2,051
Self-citationThe Kidney, Hypertension, and Obesity
Hall, J. E. (2003) · Hypertension · doi:10.1161/01.hyp.0000052314.95497.78 · Cited by 868
Self-citationObesity-related glomerulopathy: clinical and pathologic characteristics and pathogenesis
D’Agati, V. D., Chagnac, A., de Vries, A. P. J., Levi, M., Porrini, E., Herman‐Edelstein, M., & Praga, M. (2016) · Nature Reviews Nephrology · doi:10.1038/nrneph.2016.75 · Cited by 735
Obesity, kidney dysfunction and hypertension: mechanistic links
Hall, J. E., do Carmo, J. M., da Silva, A. A., Wang, Z., & Hall, M. E. (2019) · Nature Reviews Nephrology · doi:10.1038/s41581-019-0145-4 · Cited by 654
Self-citationRenal Damage in Primary Aldosteronism: Results of the PAPY Study
Rossi, G. P., Bernini, G., Desideri, G., Fabris, B., Ferri, C., Giacchetti, G., Letizia, C., Maccario, M., Mannelli, M., Matterello, M.-J., et al. (2006) · Hypertension · doi:10.1161/01.hyp.0000230444.01215.6a · Cited by 470
Disorders of body water homeostasis
Verbalis, J. G. (2003) · Best Practice & Research Clinical Endocrinology & Metabolism · doi:10.1016/s1521-690x(03)00049-6 · Cited by 457
Recommendations for Blood Pressure Measurement in Humans and Experimental Animals
Kurtz, T. W., Griffin, K. A., BIDANI, A. K., Davisson, R. L., & Hall, J. E. (2004) · Hypertension · doi:10.1161/01.hyp.0000150857.39919.cb · Cited by 262
Self-citationThe Pathophysiology of Aldosterone in the Cardiovascular System
ROCHA, R., & Funder, J. W. (2002) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2002.tb04415.x · Cited by 259
The Role of the Kidney in Hypertension
Cowley, A. W. (1996) · JAMA · doi:10.1001/jama.1996.03530440061038 · Cited by 260
Fogo, A. B., Breyer, J. A., Smith, M. C. F., et al. (1997) · Kidney International · doi:10.1038/ki.1997.29 · Cited by 247
Self-citationHypertension: Physiology and Pathophysiology
Hall, J. E., Granger, J. P., do Carmo, J. M., da Silva, A. A., Dubinion, J., George, E., Hamza, S., Speed, J., & Hall, M. E. (2012) · Comprehensive Physiology · doi:10.1002/cphy.c110058 · Cited by 232
Self-citationThe Renal Medulla and Hypertension
Cowley, A. W., Mattson, D. L., Lu, S., & Roman, R. J. (1995) · Hypertension · doi:10.1161/01.hyp.25.4.663 · Cited by 226
Aldosterone Antagonism Attenuates Obesity-Induced Hypertension and Glomerular Hyperfiltration
de Paula, R. B., da Silva, A. A., & Hall, J. E. (2004) · Hypertension · doi:10.1161/01.hyp.0000105624.68174.00 · Cited by 207
Self-citationLouis K. Dahl Memorial Lecture. Renal and cardiovascular mechanisms of hypertension in obesity.
Hall, J. E. (1994) · Hypertension · doi:10.1161/01.hyp.23.3.381 · Cited by 204
Self-citationRelative Glomerular Hyperfiltration in Primary Aldosteronism
Ribstein, J., du Cailar, G., Fesler, P., & Mimran, A. (2005) · Journal of the American Society of Nephrology · doi:10.1681/asn.2004100878 · Cited by 201
“The occurrence of escape is associated with a proportional increase in GFR and renal plasma flow by approximately 20% (15).”
BackgroundAbnormal pressure natriuresis. A cause or a consequence of hypertension?
Hall, J. E., Mizelle, H. L., Hildebrandt, D. A., & Brands, M. W. (1990) · Hypertension · doi:10.1161/01.hyp.15.6.547 · Cited by 193
“To resolve these issues and to directly test the importance of pressure natriuresis in regulating sodium balance in hypertension, we compared the chronic blood pressure and renal effects of aldosterone or Ang II infusion in dogs in which renal perfusion pressure was either permitted to increase or servo-controlled at…”
BackgroundSelf-citationRisk Factors Associated with a Low Glomerular Filtration Rate in Primary Aldosteronism
Reincke, M., Rump, L. C., Quinkler, M. O., Hahner, S., Diederich, S., Lorenz, R. L., Seufert, J., Schirpenbach, C., Beuschlein, F., Bidlingmaier, M., et al. (2008) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2008-1851 · Cited by 176
“pressure natriuresis phenomenon (16), mediated by natriuretic”
Recommendations for Blood Pressure Measurement in Humans and Experimental Animals
Kurtz, T. W., Griffin, K. A., BIDANI, A. K., Davisson, R. L., & Hall, J. E. (2005) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000158419.98675.d7 · Cited by 173
Self-citationRossi, G. P. (2019) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2019.09.057 · Cited by 167
Licorice-Induced Hypertension and Syndromes of Apparent Mineralocorticoid Excess
Walker, B. R., & Edwards, C. R. W. (1994) · Endocrinology and Metabolism Clinics of North America · doi:10.1016/s0889-8529(18)30102-6 · Cited by 153
Renal Dysfunction, Rather Than Nonrenal Vascular Dysfunction, Mediates Salt-Induced Hypertension
Hall, J. E. (2016) · Circulation · doi:10.1161/circulationaha.115.018526 · Cited by 152
Self-citationMineralocorticoid Receptors, Salt-Sensitive Hypertension, and Metabolic Syndrome
Fujita, T. (2010) · Hypertension · doi:10.1161/hypertensionaha.109.149062 · Cited by 130
Intrarenal Hemodynamics in Primary Aldosteronism before and after Treatment
Sechi, L. A., Fabio, A. D., Bazzocchi, M., et al. (2009) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2008-2245 · Cited by 129
Wang, X., Desai, K. M., Clausen, J. T., & Wu, L. (2004) · Kidney International · doi:10.1111/j.1523-1755.2004.66034.x · Cited by 126
“The kidney plays a major role in blood pressure homeostasis [22], and possibly the pathogenesis of hypertension in SHR [23] and other models of hypertension, such as DOCA-salt–sensitive hypertension [24].”
BackgroundThe renal thiazide-sensitive Na-Cl cotransporter as mediator of the aldosterone-escape phenomenon
Wang, X., Masilamani, S. M. E., Nielsen, J., et al. (2001) · Journal of Clinical Investigation · doi:10.1172/jci10366 · Cited by 121
“Aldosterone escape is dependent on increased renal vascular perfusion pressure rather than systemic factors such as changes in circulating hormone levels or renal nerve activity (10).”
BackgroundRelationship between birthweight and blood pressure in childhood
Yiu, V., Buka, S. L., Zurakowski, D., McCormick, M. C., Brenner, B. M., & Jabs, K. L. (1999) · American Journal of Kidney Diseases · doi:10.1016/s0272-6386(99)70297-0 · Cited by 118
Mechanisms of pressure natriuresis
Granger, J. P., Alexander, B. T., & Llinas, M. (2002) · Current Hypertension Reports · doi:10.1007/s11906-002-0040-3 · Cited by 117
Self-citationIwakura, Y., Morimoto, R., Kudo, M., Ono, Y., Takase, K., Seiji, K., Arai, Y., Nakamura, Y., Sasano, H., Ito, S., et al. (2013) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2013-2180 · Cited by 116
Regulation of Potassium Excretion
Malnic, G., Muto, S., & Giebisch, G. (2008) · Elsevier eBooks · doi:10.1016/b978-012088488-9.50050-4 · Cited by 105
Determinants of natriuretic peptide gene expression
McGrath, M. F., & de Bold, A. J. (2005) · Peptides · doi:10.1016/j.peptides.2004.12.022 · Cited by 102
Montani, J., & Van Vliet, B. N. (2009) · Experimental Physiology · doi:10.1113/expphysiol.2008.043299 · Cited by 100
Wu, V., Chueh, S., Chang, H., Lin, L., Liu, K., Lin, Y., Ho, Y., Lin, W., Wang, S., Huang, K., et al. (2009) · American Journal of Kidney Diseases · doi:10.1053/j.ajkd.2009.06.014 · Cited by 100
Gassman, J., Greene, T., Wright, J. T., Agodoa, L. Y. C., Bakris, G. L., Beck, G. J., Douglas, J. G., Jamerson, K., Lewis, J. B., Kutner, M., et al. (2003) · Journal of the American Society of Nephrology · doi:10.1097/01.asn.0000070080.21680.cb · Cited by 92
Mechanisms of sodium balance: total body sodium, surrogate variables, and renal sodium excretion
Bie, P. (2018) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00363.2017 · Cited by 94
“The classical results of Hall et al. (84) were part of extensive chronic studies in conscious dogs of the interaction between blood pressure changes, renin system activity, and renal sodium excretion (33, 74, 75, 77, 82–85, 109, 161), all interpreted to comply with the pressure natriuresis concept.”
BackgroundResultBallermann, B. J., Bloch, K. D., Seidman, J. G., et al. (1986) · Journal of Clinical Investigation · doi:10.1172/jci112650 · Cited by 84
Renal function curve in patients with secondary forms of hypertension.
Kimura, G., Saito, F., Kojima, S., Yoshimi, H., Abe, H., Kawano, Y., Yoshida, K., Ashida, T., Kawamura, M., & Kuramochi, M. (1987) · Hypertension · doi:10.1161/01.hyp.10.1.11 · Cited by 79
Ziomber, A., Machnik, A., Dahlmann, A., Dietsch, P., Beck, F.-X., Wagner, H., Hilgers, K. F., Luft, F. C., Eckardt, K., & Titze, J. M. (2008) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00531.2007 · Cited by 72
Purinergic Inhibition of ENaC Produces Aldosterone Escape
Stockand, J. D., Mironova, E., Bugaj, V., Rieg, T., Insel, P. A., Vallon, V., Peti‐Peterdi, J., & Pochynyuk, O. M. (2010) · Journal of the American Society of Nephrology · doi:10.1681/asn.2010040377 · Cited by 70
Yokota, N., Bruneau, B. G., de Bold, M. L. K., et al. (1994) · Journal of Clinical Investigation · doi:10.1172/jci117544 · Cited by 67
Aldosterone Blunts Tubuloglomerular Feedback by Activating Macula Densa Mineralocorticoid Receptors
Fu, Y., Hall, J. E., Lu, D., Lin, L., Manning, R. D., Cheng, L., Gomez-Sanchez, C. E., Juncos, L. A., & Liu, R. (2012) · Hypertension · doi:10.1161/hypertensionaha.111.173195 · Cited by 65
Self-citationTurban, S., Wang, X., & Knepper, M. A. (2003) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00110.2003 · Cited by 63
“On the basis of experiments by Hall and colleagues (14) in which renal perfusion pressure was prevented from increasing by a servo-null system, the aldosterone escape process appears to depend on an increase in renal perfusion pressure.”
BackgroundWang, X., Desai, K. M., Juurlink, B. H. J., de Champlain, J., & Wu, L. (2006) · Kidney International · doi:10.1038/sj.ki.5000043 · Cited by 63
Titze, J. M., Luft, F. C., Bauer, K. H., Dietsch, P., Lang, R., Veelken, R. A., Wagner, H., Eckardt, K., & Hilgers, K. F. (2006) · Hypertension · doi:10.1161/01.hyp.0000221039.17735.1a · Cited by 58
Volume natriuresis vs. pressure natriuresis
Bie, P., Wamberg, S., & Kjølby, M. (2004) · Acta Physiologica Scandinavica · doi:10.1111/j.1365-201x.2004.01323.x · Cited by 58
Control of blood pressure by the renin‐angiotensin‐aldosterone system
Hall, J. E. (1991) · Clinical Cardiology · doi:10.1002/clc.4960141802 · Cited by 57
Self-citationGonzalez-Campoy, M. J., Romero, C. J., & Knox, F. G. (1989) · Kidney International · doi:10.1038/ki.1989.51 · Cited by 56
Electrolyte disorders in cancer patients: a systematic review
Berardi, R., Torniai, M., Lenci, E., Pecci, F., Morgese, F., & Rinaldi, S. (2019) · Journal of Cancer Metastasis and Treatment · doi:10.20517/2394-4722.2019.008 · Cited by 55
“In particular, the angiotensin II arginine vasopressin (AVP) - atrial natriuretic peptide pathway is the most important mechanism of sodium balance([7]), and it is strictly associated to serum osmolality([8]).”
BackgroundRationale for the Use of Aldosterone Antagonists in Congestive Heart Failure
Rocha, R., & Williams, G. H. (2002) · Drugs · doi:10.2165/00003495-200262050-00001 · Cited by 54
“Importantly, in healthy animals and humans, there is a modulating mechanism (mineralocorticoid escape) that prevents continued sodium reabsorption beyond approximately 5 days, even with the continuing presence of aldosterone.[12] This phenomenon occurs in response to haemodynamic changes in the renal circulation.”
BackgroundMineralocorticoid escape in patients with compensated cirrhosis and portal hypertension
Villa, G. L., Salmerón, J. M., Arroyo, V., et al. (1992) · Gastroenterology · doi:10.1016/0016-5085(92)90340-5 · Cited by 55
Systemic hypertension and the kidney in black patients
Dustan, H. P., Curtis, J. J., Luke, R. G., & Rostand, S. G. (1987) · The American Journal of Cardiology · doi:10.1016/0002-9149(87)90464-4 · Cited by 54
Stanton, B. A., & Giebisch, G. (1992) · Comprehensive physiology · doi:10.1002/cphy.cp080119 · Cited by 50
Role of angiotensin AT 2 receptors in natriuresis: Intrarenal mechanisms and therapeutic potential
Carey, R. M., & Padia, S. H. (2013) · Clinical and Experimental Pharmacology and Physiology · doi:10.1111/1440-1681.12059 · Cited by 46
Control of Sodium Excretion: An Integrative Approach
Knox, F. G., & Granger, J. P. (1992) · Comprehensive physiology · doi:10.1002/cphy.cp080121 · Cited by 45
Self-citationToney, G. M., Vallon, V., & Stockand, J. D. (2011) · Current Opinion in Nephrology & Hypertension · doi:10.1097/mnh.0b013e32834db4a0 · Cited by 40
“This is when sodium excretion is elevated appropriately in the presence of a sodium load despite high levels of aldosterone [4,5].”
BackgroundRole of pressure natriuresis in long-term control of renal electrolyte excretion.
Mizelle, H. L., Montani, J. P., Hester, R. L., DIDLAKE, R. H., & Hall, J. E. (1993) · Hypertension · doi:10.1161/01.hyp.22.1.102 · Cited by 40
Self-citationNormotension, hypertension and body fluid regulation: brain and kidney
Bie, P., & Evans, R. G. (2016) · Acta Physiologica · doi:10.1111/apha.12718 · Cited by 39
“…over rates of sodium excretion spanning two orders of magnitude; (iii) particularly in renocentric contexts, it is often assumed that sodium loading causes transient elevations in arterial pressure responsible for chronic adjustments of natriuretic mechanisms (Brands 2012, Hall et al. 2012).”
BackgroundMethodInfluentialGranger, J. P., Kassab, S. E., Novak, J., Reckelhoff, J. F., Tucker, B., & Miller, M. T. (1999) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.1999.276.1.r197 · Cited by 37
“An increase in renal perfusion pressure has been shown to play an important role in offsetting the direct sodium-retaining actions of aldosterone (17).”
BackgroundInfluentialSelf-citationBeierwaltes, W. H., Harrison‐Bernard, L. M., Sullivan, J. C., & Mattson, D. L. (2012) · Comprehensive physiology · doi:10.1002/cphy.c120008 · Cited by 39
The Renin‐Angiotensin System Normal Physiology and Changes in Older Hypertensives
Hall, J. E., Coleman, T. G., & Guyton, A. C. (1989) · Journal of the American Geriatrics Society · doi:10.1111/j.1532-5415.1989.tb02245.x · Cited by 38
Self-citationAtrial Natriuretic Peptide during Mineralocorticoid Escape in the Human*
Zimmerman, R. S., Edwards, B. S., Schwab, T. R., et al. (1987) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem-64-3-624 · Cited by 36
Chronic Blood Pressure Control
Brands, M. W. (2012) · Comprehensive physiology · doi:10.1002/cphy.c100056 · Cited by 35
Renal Tubule Sodium Transporter Abundance Profiling in Rat Kidney
Knepper, M. A., Kim, G., & Masilamani, S. M. E. (2003) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2003.tb07254.x · Cited by 33
Renal damage in primary aldosteronism: Results of the PAPY study
Tuck, M. L., & Corry, D. B. (2007) · Current Hypertension Reports · doi:10.1007/s11906-007-0016-4 · Cited by 34
mPGES-1 deletion impairs aldosterone escape and enhances sodium appetite
Jia, Z., Aoyagi, T., Kohan, D. E., & Yang, T. (2010) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.90702.2008 · Cited by 32
“Aldo escape is attributed to the activation of compensatory mechanisms secondary to the increases in renal perfusion pressure (26) or extracellular volume.”
BackgroundUeda, S., Fortune, V., Bull, B. S., Valenzuela, G. J., & Longo, L. D. (1986) · American Journal of Obstetrics and Gynecology · doi:10.1016/0002-9378(86)90110-9 · Cited by 33
Nizar, J. M., Shepard, B. D., Vo, V., & Bhalla, V. (2018) · JCI Insight · doi:10.1172/jci.insight.95107 · Cited by 33
“Hall and colleagues (37, 38) elegantly demonstrated that aldosterone acts at the macula densa to disrupt tubuloglomerular feedback and increase glomerular filtration rate, promoting sodium excretion to return to sodium balance during hyperaldosteronism (i.”
BackgroundEndothelial factors in the pathogenesis and treatment of chronic kidney disease Part I
Rossi, G. P., Seccia, T. M., Barton, M., Danser, A. H. J., de Leeuw, P. W., Dhaun, N., Rizzoni, D., Rossignol, P., Ruilope, L. M., van den Meiracker, A. H., et al. (2017) · Journal of Hypertension · doi:10.1097/hjh.0000000000001599 · Cited by 33
“When infused into dogs, in which renal perfusion pressure was clamped to 19 mmHg, aldosterone (14 mg/kg per day) was found to cause hyperfiltration [43], a finding that can explain the hyperfiltration seen in human primary aldosteronism, and the apparent worsening of estimated GFR after cure of the hyperaldosteronism…”
BackgroundHusková, Z., Vaňourková, Z., Erbanová, M., et al. (2010) · Journal of Hypertension · doi:10.1097/hjh.0b013e3283345d69 · Cited by 27
Kim, D. H., Kwon, H. J., Ji, S. A., Jang, H. R., Jung, S.-H., Kim, J., Kim, J. H., Lee, J. E., Huh, W., Kim, Y.-G., et al. (2016) · Medicine · doi:10.1097/md.0000000000003930 · Cited by 26
Than, W. H., Chan, G. C., Ng, J. K., & Szeto, C. (2020) · Advances in Biomarker Sciences and Technology · doi:10.1016/j.abst.2020.09.001 · Cited by 25
Hall, M. E., & Hall, J. E. (2017) · Elsevier eBooks · doi:10.1016/b978-0-323-42973-3.00005-6 · Cited by 36
Self-citation4 Control of blood and extracellular volume
Cowley, A. W., & Roman, R. J. (1989) · Baillière s Clinical Endocrinology and Metabolism · doi:10.1016/s0950-351x(89)80007-2 · Cited by 24
Influence of angiotensin on the early progression of heart failure
Lohmeier, T. E., Mizelle, H. L., Reinhart, G. A., et al. (2000) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.2000.278.1.r74 · Cited by 24
“Measurements of GFR and RPF were made from the plasma clearances of [125I]iothalamate (Glofil, Isotex Diagnostics, Friendswood, TX) and [131I]iodohippurate (Hippuran, Syncor International, Jackson, MS), respectively, using methods previously described (14, 15, 28).”
MethodRenal sympathetic activity: A key modulator of pressure natriuresis in hypertension
Díaz-Morales, N., Baranda-Alonso, E. M., Martínez-Salgado, C., & López-Hernández, F. J. (2023) · Biochemical Pharmacology · doi:10.1016/j.bcp.2022.115386 · Cited by 24
Malnic, G., Giebisch, G., Muto, S., Wang, W., Bailey, M. A., & Satlin, L. M. (2012) · Elsevier eBooks · doi:10.1016/b978-0-12-381462-3.00049-5 · Cited by 21
Potassium supplementation ameliorates mineralocorticoid-induced sodium retention
Krishna, G. G., & Kapoor, S. C. (1993) · Kidney International · doi:10.1038/ki.1993.154 · Cited by 21
Grim, C. E. (2004) · Current Hypertension Reports · doi:10.1007/s11906-004-0045-1 · Cited by 22
Aldosterone: Renal Action and Physiological Effects
Johnston, J. G., Welch, A., Cain, B. D., Sayeski, P. P., Gumz, M. L., & Wingo, C. S. (2023) · Comprehensive physiology · doi:10.1002/cphy.c190043 · Cited by 41
Computer Models for Designing Hypertension Experiments and Studying Concepts
Guyton, A. C., Montani, J.-P., Hall, J. E., & Manning, R. D. (1988) · The American Journal of the Medical Sciences · doi:10.1097/00000441-198804000-00018 · Cited by 20
Self-citationTorresan, F., Rossitto, G., Bisogni, V., Lerco, S., Maiolino, G., Cesari, M., Zhu, R., Iacobone, M., Seccia, T. M., & Rossi, G. P. (2020) · Clinical Science · doi:10.1042/cs20200340 · Cited by 21
Escape from the Sodium-Retaining Action of Intrarenal Angiotensins II and III in the Conscious Dog*
Dickstein, G., WOODSON, J. F., LAMB, N. E., et al. (1985) · Endocrinology · doi:10.1210/endo-117-5-2160 · Cited by 19
The Kidney in Normal Pregnancy and Preeclampsia
Conrad, K. P., Gaber, L. W., & Lindheimer, M. D. (2009) · Elsevier eBooks · doi:10.1016/b978-0-12-374213-1.00017-3 · Cited by 18
The renal effects of mineralocorticoid receptor antagonists.
Bianchi, S., Batini, V., & Bigazzi, R. (2015) · International Journal of Cardiology · doi:10.1016/j.ijcard.2015.05.125 · Cited by 15
Pillai, P. R., Griffith, M. P., Schwarcz, M., & Weiss, I. A. (2019) · Cardiology in Review · doi:10.1097/crd.0000000000000281 · Cited by 17
“Interestingly, patients with PA do not develop severe volume overload in part due to a renal escape mechanism.(7) Although it had previously been thought that hypokalemia was seen in most patients with PA, it is now clear that only a minority (9–37%) of patients with PA present with hypokalemia.”
Grekin, R. J., Ling, W. D., Shenker, Y., et al. (1986) · Hypertension · doi:10.1161/01.hyp.8.6_pt_2.ii16 · Cited by 16
“Glomenilar filtration rates are increased during mineralocorticoid escape.(33) Hall et al.”
BackgroundEndocrine Causes of Hypertension in Children
Rodd, C. J., & Sockalosky, J. J. (1993) · Pediatric Clinics of North America · doi:10.1016/s0031-3955(16)38487-5 · Cited by 15
Pathophysiology, Diagnosis, and Treatment of Mineralocorticoid Disorders
Magill, S. B. (2014) · Comprehensive physiology · doi:10.1002/cphy.c130042 · Cited by 15
“the sodium-retentive effects of aldosterone and returns the Na+ balance to equilibrium (15, 134).”
Mineralocorticoid Hypertension and Hypokalemia
Khosla, N., & Hogan, D. (2006) · Seminars in Nephrology · doi:10.1016/j.semnephrol.2006.10.004 · Cited by 14
Zeng, Z.-P., Naruse, M., Naruse, K., et al. (1991) · Endocrinology · doi:10.1210/endo-128-1-226 · Cited by 14
Integration and regulation of cardiovascular function.
Hall, J. E. (1999) · AJP Advances in Physiology Education · doi:10.1152/advances.1999.277.6.s174 · Cited by 13
“Although this ‘‘escape’’ has been traditionally explained by increased formation of various natriuretic systems stimulated by volume expansion, such as ANP, it appears to be due mainly to the rise in blood pressure and the resultant pressure natriuresis (5).”
BackgroundSelf-citationMechanisms of sodium‐mediated injury in cardiovascular disease: old play, new scripts
Rossitto, G., & Delles, C. (2021) · FEBS Journal · doi:10.1111/febs.16155 · Cited by 12
Kurtz, T. W., Griffin, K. A., BIDANI, A. K., Davisson, R. L., & John, E. B. (2005) · Cited by 12
Seeliger, E., Boemke, W., Corea, M., et al. (1997) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.1997.273.2.r646 · Cited by 12
Clinical Aspects of Body Fluid Homeostasis in Humans
Verbalis, J. G. (1990) · Handbook of behavioral neurobiology · doi:10.1007/978-1-4613-0577-4_16 · Cited by 12
Primary and Secondary Hypertension
Blumenfeld, J. D., Liu, F., & Laragh, J. H. (2012) · Elsevier eBooks · doi:10.1016/b978-1-4160-6193-9.10046-6 · Cited by 11
Low-Dose Nitric Oxide Inhibition Produces a Negative Sodium Balance in Conscious Dogs
Seeliger, E., Persson, P. B., Boemke, W., MOLLENHAUER, G. D., Nafz, B., & Reinhardt, H. W. (2001) · Journal of the American Society of Nephrology · doi:10.1681/asn.v1261128 · Cited by 11
Sechi, L. A., & Catena, C. (2009) · American Journal of Kidney Diseases · doi:10.1053/j.ajkd.2009.08.004 · Cited by 10
Physiology and Pathophysiology of Hypertension
Hall, J. E., Granger, J. P., & Hall, M. E. (2012) · Elsevier eBooks · doi:10.1016/b978-0-12-381462-3.00039-2 · Cited by 11
Self-citationThe Kidney in Normal Pregnancy and Preeclampsia
Conrad, K. P., Stillman, I. E., & Lindheimer, M. D. (2014) · Elsevier eBooks · doi:10.1016/b978-0-12-407866-6.00016-x · Cited by 10
Natriuretic Peptides and Salt Sensitivity
Villarreal, D., & Freeman, R. H. (1997) · Humana Press eBooks · doi:10.1007/978-1-4612-3960-4_14 · Cited by 9
Metadata
- Authors
- Hall, J. E., Granger, J. P., Smith, M. J., & Premen, A. J.
- ORCID
- Hall, J E
- Venue
- Hypertension
- Published
- 1984-03
- Volume
- 6
- Issue
- 2_pt_2
- Pages
- I183-92
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2063605611
- Cited by
- 153
- References
- 0
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2023: 4 · 2022: 5 · 2021: 2 · 2020: 3 · 2019: 5 · 2018: 6 · 2017: 3 · 2016: 4 · 2015: 3 · 2014: 4 · 2013: 3 · 2012: 10
- FWCI
- 2.86
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Keywords
- aldosterone escape, renal hemodynamics, renal artery pressure, sodium retention, sodium excretion, fractional excretion of sodium, glomerular filtration rate, sodium balance, volume expansion, ascites, aortic occlusion, mean arterial pressure
- MeSH terms
- Aldosterone, Animals, Blood Pressure, Dogs, Glomerular Filtration Rate, Infusions, Parenteral, Kidney, Perfusion, Renal Circulation, Sodium
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
