Role of Angiotensinogen and Relative Aldosterone Excess in Salt-Sensitive Hypertension
2012; Lippincott Williams & Wilkins; Volume: 59; Issue: 6 Linguagem: Inglês
10.1161/hypertensionaha.112.195230
ISSN1524-4563
AutoresMichihiro Satoh, Masahiro Kikuya, Takayoshi Ohkubo, Yutaka Imai,
Tópico(s)Blood Pressure and Hypertension Studies
ResumoHomeHypertensionVol. 59, No. 6Role of Angiotensinogen and Relative Aldosterone Excess in Salt-Sensitive Hypertension Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBRole of Angiotensinogen and Relative Aldosterone Excess in Salt-Sensitive Hypertension Michihiro Satoh and Masahiro Kikuya Takayoshi Ohkubo Yutaka Imai Michihiro SatohMichihiro Satoh Department of Planning for Drug Development and Clinical Evaluation Tohoku University Graduate School of Pharmaceutical Sciences and Medicine Sendai, Japan (Satoh, Kikuya) and Masahiro KikuyaMasahiro Kikuya Department of Planning for Drug Development and Clinical Evaluation Tohoku University Graduate School of Pharmaceutical Sciences and Medicine Sendai, Japan (Satoh, Kikuya) Takayoshi OhkuboTakayoshi Ohkubo Department of Planning for Drug Development and Clinical Evaluation Tohoku University Graduate School of Pharmaceutical Sciences and Medicine Sendai, Japan Department of Health Science Shiga University of Medical Science Otsu, Japan (Ohkubo) Yutaka ImaiYutaka Imai Department of Planning for Drug Development and Clinical Evaluation Tohoku University Graduate School of Pharmaceutical Sciences and Medicine Sendai, Japan (Imai) Originally published30 Apr 2012https://doi.org/10.1161/HYPERTENSIONAHA.112.195230Hypertension. 2012;59:e57Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2012: Previous Version 1 To the Editor:We read with great interest the article by Michel et al.1 They demonstrated that circulating angiotensinogen concentration (AGT) was positively associated with aldosterone level and blood pressure in subjects of African ancestry with high urinary Na/K ratio. Their findings may elucidate one of the key mechanisms of salt-sensitive hypertension. We have several comments regarding their work.Compared with aldosterone level alone, aldosterone/renin ratio (ARR) is more reproducible and could be an index for inappropriate aldosterone activity and salt sensitivity. In a recent publication from their group, urinary Na/K ratio was positively associated with blood pressure levels in subjects of African ancestry with high ARR.2 We also reported that high ARR but not aldosterone level was significantly associated with hypertension diagnosed based on home blood pressure measurement in a Japanese general population with high Na intake.3 These results2,3 suggest that high ARR, that is, relative aldosterone excess, may be attributable to salt-sensitive hypertension in subjects of Asian and African ancestry. In relative aldosterone excess, aldosterone does not fully decrease, although renin activity is suppressed by sodium-volume overload; this mechanism is supposed to be responsible for salt-sensitive hypertension caused by inappropriate sodium and fluid retention. Michel et al1 noted that AGT is an important determinant of renin-angiotensin-aldosterone system activation under the condition of renin suppression. Thus, we presume that the association of high ARR with salt-sensitive hypertension may partly be mediated by AGT. However, the detailed relationships between ARR and blood pressure or AGT were not described in their study.1In patients with salt-sensitive hypertension, it is reported that nocturnal blood pressure decline is diminished, which is generally referred to as a "nondipping" pattern.4 We reported previously that high ARR was related to a nondipping pattern in individuals with high Na excretion, supporting the hypothesis that relative aldosterone excess may cause salt-sensitive hypertension.5We, therefore, would like to know the relationship between AGT and ARR among their subjects of African ancestry with high urinary Na/K ratio. For a more detailed understanding, we would also like to know whether the association between ARR and blood pressure differs before and after adjustment for AGT. Furthermore, if they have ambulatory blood pressure monitoring data, it would be very interesting to see the association between AGT and the nondipping pattern, as well as with blood pressure level. This information could also help clarify the role of AGT in the renin-angiotensin system and in salt-sensitive hypertension.Michihiro SatohMasahiro Kikuya Department of Planning for Drug Development and Clinical Evaluation Tohoku University Graduate School of Pharmaceutical Sciences and Medicine Sendai, JapanTakayoshi Ohkubo Department of Planning for Drug Development and Clinical Evaluation Tohoku University Graduate School of Pharmaceutical Sciences and Medicine Sendai, Japan Department of Health Science Shiga University of Medical Science Otsu, JapanYutaka Imai Department of Planning for Drug Development and Clinical Evaluation Tohoku University Graduate School of Pharmaceutical Sciences and Medicine Sendai, JapanSources of FundingThis article was supported in part by Grants for Scientific Research (18390192, 18590587, 19590929, 19790423, 20590629, 21390201, 21591016, 22590767, 22790556, 22890017, 23249036, and 23790242) from the Ministry of Education, Culture, Sports, Science, and Technology, Japan; Grant-in-Aid (H18-Junkankitou[Seishuu]-Ippan-012, H20-Junkankitou[Seishuu]-Ippan-009, 013, and H23-Junkankitou [Senshuu]-Ippan-005) from the Ministry of Health, Labor and Welfare, Health and Labor Sciences Research Grants, Japan; Grant-in-Aid for Japan Society for the Promotion of Science (JSPS) fellows (18.54042, 19.7152, 20.7198, 20.7477, and 20.54043); Health Science Research Grants and Medical Technology Evaluation Research Grants from the Ministry of Health, Labor and Welfare, Japan; Japan Arteriosclerosis Prevention Fund; Biomedical Innovation Grants; a Grant from the Miso Central Institute, Tokyo, Japan; and a Grant from the Sendai Knowledge Cluster Initiative, Sendai, Japan.DisclosuresNone.FootnotesLetters to the Editor will be published, if suitable, as space permits. They should not exceed 1000 words (typed double-spaced) in length and may be subject to editing or abridgment. References 1. Michel FS, Norton GR, Majane OH, Badenhorst M, Vengethasamy L, Paiker J, Maseko MJ, Sareli P, Woodiwiss AJ. Contribution of circulating angiotensinogen concentrations to variations in aldosterone and blood pressure in a group of African ancestry depends on salt intake. Hypertension. 2012; 59:62–69.LinkGoogle Scholar2. Scott L, Woodiwiss AJ, Maseko MJ, Veliotes DG, Majane OH, Paiker J, Sareli P, Norton GR. Aldosterone-to-renin ratio and the relationship between urinary salt excretion and blood pressure in a community of African ancestry. Am J Hypertens. 2011; 24:951–957.CrossrefMedlineGoogle Scholar3. Satoh M, Kikuya M, Hara A, Ohkubo T, Mori T, Metoki H, Utsugi MT, Hirose T, Obara T, Inoue R, Asayama K, Totsune K, Hoshi H, Satoh H, Imai Y. Aldosterone-to-renin ratio and home blood pressure in subjects with higher and lower sodium intake: the Ohasama Study. Hypertens Res. 2011; 34:361–366.CrossrefMedlineGoogle Scholar4. Uzu T, Kazembe FS, Ishikawa K, Nakamura S, Inenaga T, Kimura G. High sodium sensitivity implicates nocturnal hypertension in essential hypertension. Hypertension. 1996; 28:139–142.LinkGoogle Scholar5. Satoh M, Kikuya M, Ohkubo T, Mori T, Metoki H, Hashimoto T, Hara A, Utsugi MT, Hirose T, Obara T, Inoue R, Asayama K, Kanno A, Totsune K, Hoshi H, Satoh H, Imai Y. Aldosterone-to-renin ratio and nocturnal blood pressure decline in a general population: the Ohasama Study. J Hypertens. 2011; 29:1940–1947.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Faulkner J (2021) Obesity-associated cardiovascular risk in women: hypertension and heart failure, Clinical Science, 10.1042/CS20210384, 135:12, (1523-1544), Online publication date: 25-Jun-2021. Clemmer J, Faulkner J, Mullen A, Butler K and Hester R (2019) Sex-specific responses to mineralocorticoid receptor antagonism in hypertensive African American males and females, Biology of Sex Differences, 10.1186/s13293-019-0238-6, 10:1, Online publication date: 1-Dec-2019. Faulkner J, Harwood D, Bender L, Shrestha L, Brands M, Morwitzer M, Kennard S, Antonova G and Belin de Chantemèle E (2018) Lack of Suppression of Aldosterone Production Leads to Salt-Sensitive Hypertension in Female but Not Male Balb/C Mice, Hypertension, 72:6, (1397-1406), Online publication date: 1-Dec-2018. Huang P, Chen S, Wang Y, Liu J, Yao Q, Huang Y, Li H, Zhu M, Wang S, Li L, Tang C, Tao Y, Yang G, Du J and Jin H (2015) Down-regulated CBS/H2S pathway is involved in high-salt-induced hypertension in Dahl rats, Nitric Oxide, 10.1016/j.niox.2015.01.004, 46, (192-203), Online publication date: 1-Apr-2015. Satoh M, Kikuya M, Hosaka M, Asayama K, Inoue R, Metoki H, Tsubota-Utsugi M, Hara A, Hirose T, Obara T, Mori T, Totsune K, Hoshi H, Mano N, Imai Y and Ohkubo T (2014) Association of Aldosterone-to-Renin Ratio With Hypertension Differs by Sodium Intake: The Ohasama Study, American Journal of Hypertension, 10.1093/ajh/hpu115, 28:2, (208-215), Online publication date: 1-Feb-2015. Satoh M, Hosaka M, Asayama K, Kikuya M, Inoue R, Metoki H, Utsugi M, Hara A, Hirose T, Obara T, Mori T, Totsune K, Hoshi H, Mano N, Imai Y and Ohkubo T (2014) Aldosterone-to-renin ratio and nocturnal blood pressure decline assessed by self-measurement of blood pressure at home: the Ohasama Study, Clinical and Experimental Hypertension, 10.3109/10641963.2014.892121, 36:2, (108-114), Online publication date: 1-Apr-2014. Woodiwiss A and Norton G (2012) Response to Role of Angiotensinogen and Relative Aldosterone Excess in Salt-Sensitive Hypertension, Hypertension, 59:6, (e58-e58), Online publication date: 1-Jun-2012. June 2012Vol 59, Issue 6 Advertisement Article InformationMetrics © 2012 American Heart Association, Inc.https://doi.org/10.1161/HYPERTENSIONAHA.112.195230PMID: 22547444 Originally publishedApril 30, 2012 PDF download Advertisement SubjectsClinical StudiesEpidemiologyHypertension
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