Renal Sinus Adiposity and Hypertension
2010; Lippincott Williams & Wilkins; Volume: 56; Issue: 5 Linguagem: Inglês
10.1161/hypertensionaha.110.158535
ISSN1524-4563
AutoresAlbert H.A. Mazairac, Jaap A. Joles,
Tópico(s)Thermoregulation and physiological responses
ResumoHomeHypertensionVol. 56, No. 5Renal Sinus Adiposity and Hypertension Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBRenal Sinus Adiposity and Hypertension Albert H.A. Mazairac and Jaap A. Joles Albert H.A. MazairacAlbert H.A. Mazairac From the Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, The Netherlands. and Jaap A. JolesJaap A. Joles From the Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, The Netherlands. Originally published13 Sep 2010https://doi.org/10.1161/HYPERTENSIONAHA.110.158535Hypertension. 2010;56:814–815Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: September 13, 2010: Previous Version 1 Obesity, a global health problem, has an ever increasing prevalence.1 Because excess weight is a major risk factor for high blood pressure, this results in a continuous rise in the prevalence of hypertension.2 In this issue of Hypertension, Chughtai et al3 identified a potential pathogenic link between renal sinus adiposity and hypertension in humans.Adipose tissue can be divided into compartments that carry a different metabolic risk. Thoracic and intra-abdominal adipose tissue have a strong relation with hypertension,4 whereas subcutaneous and thigh intermuscular fat tissue seem less important.5,6 Chughtai et al3 assessed the relation between the amount of renal sinus fat and hypertension. The renal sinus is the cavity within the concave border of the kidney. Other than fat, this sinus is composed of renal vessels, calices, nerve tissue, and lymphatic channels. In middle-aged and elderly individuals at risk for cardiovascular events (N=205), Chughtai et al3 showed a quantitative relation between renal sinus fat, measured with single-section MRI, and hypertension. The study had a cross-sectional design, so cause-effect relations could not be identified. Potential pathophysiological mechanisms may, however, be deduced.Obesity can lead to hypertension via pathways that stimulate sympathetic nerve activity (SNA), the renin-angiotensin-aldosterone system, and physical compression of the kidneys, all of which can cause sodium retention.2 Fat tissue has been identified as an important endocrine organ in which adipocytes secrete angiotensinogen, angiotensin II, and leptin.7 Leptin stimulates SNA.8 Norepinephrine levels are elevated in obese patients, partly because of a high caloric intake that leads to stimulation of SNA2 but perhaps also because of renal hypoxia. In patients with sleep apnea, SNA, as well as the renin-angiotensin-aldosterone system, may be further stimulated by renal hypoxia.9 Experimental evidence exists that sodium retention in obesity might be driven not only by increased renal SNA but also by increased responsiveness of the kidney to renal SNA.10 This suggests that, during increased renal SNA, renal sinus adiposity, for instance, by amplifying the decrease in medullary blood flow, might exacerbate renal hypoxia. Because renal hypoxia as such increases renal SNA, it is conceivable that renal sinus adiposity initiates a detrimental positive feedback on blood pressure control.Insulin resistance might also form a link between obesity and hypertension, because it may lead to sodium retention and an increase in SNA.11 However, the evidence to support this is mainly from experiments in rodents, and conflicting data have been found in humans. Perivascular adipose tissue may have a direct effect on vascular function and insulin sensitivity.12 However, other than such general effects, renal sinus adiposity may influence renal function and blood pressure directly by local physical constraints (Figure). Experiments using renal vein constriction have demonstrated that sodium retention can also be the result of increased renal interstitial pressure.13Download figureDownload PowerPointFigure. Renal sinus adiposity and hypertension: potential mechanisms.Weight gain is associated with renal hyalinosis.14 Expansion of the renal extracellular matrix can lead to compression of renal blood vessels and tubules attributed to the increased interstitial fluid hydrostatic pressure.15 This may slow the flow of blood and urine through the papilla, which could lead to a rightward shift of the pressure-natriuresis relation. A vicious circle can subsequently arise as the higher blood pressure again induces renal hyalinosis. Renal sinus fat may also cause hypertension by compression of the collecting ducts or veins.15,16 Venous constriction has been shown to lower glomerular filtration rate, urine volume, and osmolality and solute excretion.16Finally, differences in adipocyte function have been described between subcutaneous and visceral fat.17 It might be that renal sinus fat as an exocrine tissue differs from other intraperitoneal fat, but it seems more plausible, as extensively discussed by Chughtai et al,3 that its specific relation with hypertension is attributable to mechanical rather than exocrine effects, as suggested previously.7Assessment of renal sinus fat might help to identify patients with hypertension who would benefit most from weight loss. It has been suggested that dietary changes, notably, reducing salt intake, render more effect than weight loss itself.18 However, studies by Rocchini et al19 have shown that weight loss corrects the pressure-natriuresis relation. Recently, a large population study from China demonstrated that salt sensitivity was linearly related to the number of metabolic risk factors20 and, thus, to the degree of obesity. Hence, salt sensitivity of blood pressure may be a function of renal sinus adiposity.To assess whether a cause-effect relation indeed exists, future clinical studies should use weight loss programs to evaluate the relation between renal sinus fat and blood pressure in a prospective design. Experimental studies should assess whether decreasing renal sinus adiposity, for instance, by careful local liposuction, lowers blood pressure independent of changes in other fat compartments.The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.DisclosuresNone.FootnotesCorrespondence to Jaap A. Joles, Nephrology and Hypertension, University Medical Center Utrecht, PO Box 85500, 3508 GA Utrecht, The Netherlands. E-mail [email protected] References 1 World Health Organization. Global Strategy on Diet, Physical Activity and Health. Geneva, Switzerland: World Health Organization; 2004.Google Scholar2 Hall JE. The kidney, hypertension, and obesity. Hypertension. 2003; 41: 625–633.LinkGoogle Scholar3 Chughtai HL, Morgan TM, Rocco M, Stacey B, Brinkley TE, Ding J, Nicklas B, Hamilton C, Hundley WG. Renal sinus fat and poor blood pressure control in middle-aged and elderly individuals at risk for cardiovascular events. Hypertension. 2010; 56: 901–906.LinkGoogle Scholar4 Sironi AM, Gastaldelli A, Mari A, Ciociaro D, Positano V, Buzzigoli E, Ghione S, Turchi S, Lombardi M, Ferrannini E. Visceral fat in hypertension: influence on insulin resistance and β-cell function. Hypertension. 2004; 44: 127–133.LinkGoogle Scholar5 Fox CS, Massaro JM, Hoffmann U, Pou KM, Maurovich-Horvat P, Liu CY, Vasan RS, Murabito JM, Meigs JB, Cupples LA, D'Agostino RB Sr, O'Donnell CJ. 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Hypertension. 2004; 43: 518–524.LinkGoogle Scholar10 Michaels S, Eppel GA, Burke SL, Head GA, Armitage J, Carroll JF, Malpas SC, Evans RG. Altered responsiveness of the kidney to activation of the renal nerves in fat-fed rabbits. Am J Physiol Regul Integr Comp Physiol. 2009; 296: R1889–R1896.CrossrefMedlineGoogle Scholar11 Reaven GM, Hoffman BB. A role for insulin in the aetiology and course of hypertension? Lancet. 1987; 2: 435–437.CrossrefMedlineGoogle Scholar12 Eringa EC, Bakker W, Smulders YM, Serne EH, Yudkin JS, Stehouwer CD. Regulation of vascular function and insulin sensitivity by adipose tissue: focus on perivascular adipose tissue. Microcirculation. 2007; 14: 389–402.CrossrefMedlineGoogle Scholar13 Burnett JC Jr, Knox FG. Renal interstitial pressure and sodium excretion during renal vein constriction. Am J Physiol. 1980; 238: F279–F282.MedlineGoogle Scholar14 Dwyer TM, Banks SA, Alonso-Galicia M, Cockrell K, Carroll JF, Bigler SA, Hall JE. Distribution of renal medullary hyaluronan in lean and obese rabbits. Kidney Int. 2000; 58: 721–729.CrossrefMedlineGoogle Scholar15 Dwyer TM, Bigler SA, Moore NA, Carroll JF, Hall JE. The altered structure of renal papillary outflow tracts in obesity. Ultrastruct Pathol. 2000; 24: 251–257.CrossrefMedlineGoogle Scholar16 Stolarczyk J, Carone FA. Effects of renal lymphatic occlusion and venous constriction on renal function. Am J Pathol. 1975; 78: 285–296.MedlineGoogle Scholar17 Wajchenberg BL, Giannella-Neto D, da Silva ME, Santos RF. Depot-specific hormonal characteristics of subcutaneous and visceral adipose tissue and their relation to the metabolic syndrome. Horm Metab Res. 2002; 34: 616–621.CrossrefMedlineGoogle Scholar18 Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM, Bray GA, Vogt TM, Cutler JA, Windhauser MM, Lin PH, Karanja N. A clinical trial of the effects of dietary patterns on blood pressure: DASH Collaborative Research Group. N Engl J Med. 1997; 336: 1117–1124.CrossrefMedlineGoogle Scholar19 Rocchini AP, Key J, Bondie D, Chico R, Moorehead C, Katch V, Martin M. The effect of weight loss on the sensitivity of blood pressure to sodium in obese adolescents. N Engl J Med. 1989; 321: 580–585.CrossrefMedlineGoogle Scholar20 Chen J, Gu D, Huang J, Rao DC, Jaquish CE, Hixson JE, Chen CS, Chen J, Lu F, Hu D, Rice T, Kelly TN, Hamm LL, Whelton PK, He J. Metabolic syndrome and salt sensitivity of blood pressure in non-diabetic people in China: a dietary intervention study. Lancet. 2009; 373: 829–835.CrossrefMedlineGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetailsCited By Spit K, Muskiet M, Tonneijck L, Smits M, Kramer M, Joles J, de Boer A and van Raalte D (2019) Renal sinus fat and renal hemodynamics: a cross-sectional analysis, Magnetic Resonance Materials in Physics, Biology and Medicine, 10.1007/s10334-019-00773-z, 33:1, (73-80), Online publication date: 1-Feb-2020. Aryee C, Owiredu W, Osei-Yeboah J, Owusu-Dabo E, Laing E and Owusu I (2016) An Analysis of Anthropometric Indicators and Modifiable Lifestyle Parameters Associated with Hypertensive Nephropathy, International Journal of Hypertension, 10.1155/2016/6598921, 2016, (1-14), . Snyder S and Gangeri N (2016) Obesity, Cardiometabolic Risk, and Chronic Kidney Disease Obesity, 10.1007/978-3-319-19821-7_14, (181-198), . Pijacka W, Clifford B, Tilburgs C, Joles J, Langley-Evans S and McMullen S (2015) Protective role of female gender in programmed accelerated renal aging in the rat, Physiological Reports, 10.14814/phy2.12342, 3:4, (e12342), Online publication date: 1-Apr-2015. CHENG B, CAI Q, WU Y, ZHAO Y, GUO Q, LI G, ZHANG X, ZHANG A and NIU Y (2014)(2014) Primary renal sinus tumor: Three case reports with a review of the literature, Oncology Letters, 10.3892/ol.2014.2729, 9:2, (829-832), Online publication date: 1-Feb-2015. November 2010Vol 56, Issue 5 Advertisement Article InformationMetrics https://doi.org/10.1161/HYPERTENSIONAHA.110.158535PMID: 20837879 Originally publishedSeptember 13, 2010 PDF download Advertisement SubjectsComputerized Tomography (CT)EpidemiologyObesity
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