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Urinary angiotensin-converting enzyme 2 in hypertensive patients may be increased by olmesartan, an angiotensin II receptor blocker.
Am J Hypertens. 2015 Jan; 28(1):15-21.AJ

Abstract

BACKGROUND

Angiotensin-converting enzyme 2 (ACE2) is highly expressed in the kidney and converts angiotensin (Ang) II to Ang-(1-7), a renoprotective peptide. Urinary ACE2 has been shown to be elevated in patients with chronic kidney disease. However, the effects of antihypertensive agents on urinary ACE2 remain unclear.

METHODS

Of participants in the Tanno-Sobetsu cohort study in 2011 (n = 617), subjects on no medication (n = 101) and hypertensive patients treated with antihypertensive agents, including the calcium channel blockers amlodipine and long-acting nifedipine; the ACE inhibitor enalapril; and the Ang II receptor blockers losartan, candesartan, valsartan, telmisartan, and olmesartan, for more than 1 year (n = 100) were enrolled, and urinary ACE2 level was measured.

RESULTS

Glucose and hemoglobin A1c were significantly higher in patients treated with enalapril, telmisartan or olmesartan than in the control subjects. Urinary albumin-to-creatinine ratio (UACR) was significantly higher in patients treated with enalapril than in the control subjects. Urinary ACE2 level was higher in the olmesartan-treated group, but not the other treatment groups, than in the control group. Urinary ACE2 level was positively correlated with systolic blood pressure (r = 0.211; P = 0.003), UACR (r = 0.367; P < 0.001), and estimated salt intake (r = 0.260; P < 0.001). Multivariable regression analysis after adjustment of age, sex, and the correlated indices showed that the use of olmesartan was an independent predictor of urinary ACE2 level.

CONCLUSIONS

In contrast with other antihypertensive drugs, olmesartan may uniquely increase urinary ACE2 level, which could potentially offer additional renoprotective effects.

Authors+Show Affiliations

Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan; furuhasi@sapmed.ac.jp.Department of Nephrology, Teine Keijinkai Hospital, Sapporo, Japan;Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan;Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan;Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan;Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan;Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan;Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan;Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan;Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan; Department of Educational Development, Sapporo Medical University Center for Medical Education, Sapporo, Japan;Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan; Department of Public Health, Sapporo Medical University School of Medicine, Sapporo, Japan;Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan;Department of Nephrology, Teine Keijinkai Hospital, Sapporo, Japan;Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan; Department of Nursing, Division of Medical and Behavioral Subjects, Sapporo Medical University School of Health Sciences, Sapporo, Japan;Sapporo Nishimaruyama Hospital, Sapporo, Japan;Sapporo Medical University, Sapporo, Japan.Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan;

Pub Type(s)

Comparative Study
Journal Article
Observational Study

Language

eng

PubMed ID

24842388

Citation

Furuhashi, Masato, et al. "Urinary Angiotensin-converting Enzyme 2 in Hypertensive Patients May Be Increased By Olmesartan, an Angiotensin II Receptor Blocker." American Journal of Hypertension, vol. 28, no. 1, 2015, pp. 15-21.
Furuhashi M, Moniwa N, Mita T, et al. Urinary angiotensin-converting enzyme 2 in hypertensive patients may be increased by olmesartan, an angiotensin II receptor blocker. Am J Hypertens. 2015;28(1):15-21.
Furuhashi, M., Moniwa, N., Mita, T., Fuseya, T., Ishimura, S., Ohno, K., Shibata, S., Tanaka, M., Watanabe, Y., Akasaka, H., Ohnishi, H., Yoshida, H., Takizawa, H., Saitoh, S., Ura, N., Shimamoto, K., & Miura, T. (2015). Urinary angiotensin-converting enzyme 2 in hypertensive patients may be increased by olmesartan, an angiotensin II receptor blocker. American Journal of Hypertension, 28(1), 15-21. https://doi.org/10.1093/ajh/hpu086
Furuhashi M, et al. Urinary Angiotensin-converting Enzyme 2 in Hypertensive Patients May Be Increased By Olmesartan, an Angiotensin II Receptor Blocker. Am J Hypertens. 2015;28(1):15-21. PubMed PMID: 24842388.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Urinary angiotensin-converting enzyme 2 in hypertensive patients may be increased by olmesartan, an angiotensin II receptor blocker. AU - Furuhashi,Masato, AU - Moniwa,Norihito, AU - Mita,Tomohiro, AU - Fuseya,Takahiro, AU - Ishimura,Shutaro, AU - Ohno,Kohei, AU - Shibata,Satoru, AU - Tanaka,Marenao, AU - Watanabe,Yuki, AU - Akasaka,Hiroshi, AU - Ohnishi,Hirofumi, AU - Yoshida,Hideaki, AU - Takizawa,Hideki, AU - Saitoh,Shigeyuki, AU - Ura,Nobuyuki, AU - Shimamoto,Kazuaki, AU - Miura,Tetsuji, Y1 - 2014/05/18/ PY - 2014/5/21/entrez PY - 2014/5/21/pubmed PY - 2015/7/22/medline KW - angiotensin II receptor blocker KW - angiotensin-converting enzyme 2 KW - blood pressure KW - hypertension KW - olmesartan KW - urinary protein. KW - urine SP - 15 EP - 21 JF - American journal of hypertension JO - Am. J. Hypertens. VL - 28 IS - 1 N2 - BACKGROUND: Angiotensin-converting enzyme 2 (ACE2) is highly expressed in the kidney and converts angiotensin (Ang) II to Ang-(1-7), a renoprotective peptide. Urinary ACE2 has been shown to be elevated in patients with chronic kidney disease. However, the effects of antihypertensive agents on urinary ACE2 remain unclear. METHODS: Of participants in the Tanno-Sobetsu cohort study in 2011 (n = 617), subjects on no medication (n = 101) and hypertensive patients treated with antihypertensive agents, including the calcium channel blockers amlodipine and long-acting nifedipine; the ACE inhibitor enalapril; and the Ang II receptor blockers losartan, candesartan, valsartan, telmisartan, and olmesartan, for more than 1 year (n = 100) were enrolled, and urinary ACE2 level was measured. RESULTS: Glucose and hemoglobin A1c were significantly higher in patients treated with enalapril, telmisartan or olmesartan than in the control subjects. Urinary albumin-to-creatinine ratio (UACR) was significantly higher in patients treated with enalapril than in the control subjects. Urinary ACE2 level was higher in the olmesartan-treated group, but not the other treatment groups, than in the control group. Urinary ACE2 level was positively correlated with systolic blood pressure (r = 0.211; P = 0.003), UACR (r = 0.367; P < 0.001), and estimated salt intake (r = 0.260; P < 0.001). Multivariable regression analysis after adjustment of age, sex, and the correlated indices showed that the use of olmesartan was an independent predictor of urinary ACE2 level. CONCLUSIONS: In contrast with other antihypertensive drugs, olmesartan may uniquely increase urinary ACE2 level, which could potentially offer additional renoprotective effects. SN - 1941-7225 UR - https://www.unboundmedicine.com/medline/citation/24842388/full_citation L2 - https://academic.oup.com/ajh/article-lookup/doi/10.1093/ajh/hpu086 DB - PRIME DP - Unbound Medicine ER -