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      Urinary Angiotensin-Converting Enzyme 2 in Hypertensive Patients May Be Increased by Olmesartan, an Angiotensin II Receptor Blocker

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          Abstract

          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.

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          The angiotensin-converting enzyme gene family: genomics and pharmacology.

          Anthony Turner, Nigel Hooper (2002)
          Modulation of the renin-angiotensin system (RAS), and particularly inhibition of angiotensin-converting enzyme (ACE), a zinc metallopeptidase, has long been a prime strategy in the treatment of hypertension. However, other angiotensin metabolites are gaining in importance as our understanding of the RAS increases. Recently, genomic approaches have identified the first human homologue of ACE, termed ACEH (or ACE2). ACEH differs in specificity and physiological roles from ACE, which opens a potential new area for discovery biology. The gene that encodes collectrin, a homologue of ACEH, is upregulated in response to renal injury. Collectrin lacks a catalytic domain, which indicates that there is more to ACE-like function than simple peptide hydrolysis.
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            ACE2 inhibition worsens glomerular injury in association with increased ACE expression in streptozotocin-induced diabetic mice.

            Minghao Ye, Y Kanwar, J Lloveras … (2007)
            Angiotensin converting enzyme 2 (ACE2) is localized to the glomerular epithelial cells. Since ACE2 promotes the degradation of angiotensin II, a decrease in ACE2 activity could lead to the development of glomerular injury. We gave a specific ACE2 inhibitor, MLN-4760, for 4 weeks to mice rendered diabetic with streptozotocin. The urinary albumin/creatinine ratio was increased along with expansion of the glomerular matrix in diabetic mice treated with the inhibitor compared to the vehicle-treated mice. Glomerular staining of ACE was increased in the diabetic group and was further significantly increased in the diabetic group treated with MLN-4760. In renal vessels, ACE expression was also increased in the diabetic mice and, again, further increased in those diabetic mice treated with the ACE2 inhibitor. Our study shows that chronic pharmacologic ACE2 inhibition worsens glomerular injury in streptozotocin-induced diabetic mice in association with increased ACE expression.
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              Report of the Working Group for Dietary Salt Reduction of the Japanese Society of Hypertension: (2) Assessment of salt intake in the management of hypertension.

              Katsuyuki Ando, Hideo Matsuura, Hirotsugu Ueshima … (2007)
              Restriction of dietary salt is widely recommended in the management of hypertension, but assessment of individual salt intake has drawn little attention. The understanding of salt intake is important as a guide for optimizing salt-restriction strategies. However, precise evaluation of salt intake is difficult. More reliable methods are more difficult to perform, whereas easier methods are less reliable. Thus, the method to assess salt intake should be determined as the situation demands. The Working Group for Dietary Salt Reduction of the Japanese Society of Hypertension recommends the assessment of individual salt intake using one of the following methods in the management of hypertension. 1) The measurement of the sodium (Na) excretion from 24-h urine sampling or nutritionist's analysis of the dietary contents, which are reliable but difficult to perform, are suitable for facilities specializing in the treatment of hypertension. 2) Estimation of the Na excretion from the Na/creatinine (Cr) ratio in spot urine is less reliable but practical and is suitable for general medical facilities. 3) Estimation using an electronic salt sensor equipped with a calculation formula is also less reliable but is simple enough that patients can use it themselves. The patients are considered to be compliant with the salt-restriction regimen if salt intake measured by whichever method is less than 6 g (100 mmol)/day.
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                Author and article information

                Journal
                Title: American Journal of Hypertension
                Abbreviated Title: American Journal of Hypertension
                Publisher: Oxford University Press (OUP)
                ISSN (Print): 0895-7061
                ISSN (Electronic): 1941-7225
                Publication date Created: December 10 2014
                Publication date Created: January 01 2015
                Publication date (Electronic): May 18 2014
                Publication date (Print): January 01 2015
                Volume: 28
                Issue: 1
                Pages: 15-21
                Article
                DOI: 10.1093/ajh/hpu086
                PubMed ID: 24842388
                SO-VID: 9e63a3e1-9a4a-470d-9532-2f5abb6f8f6a
                Copyright © © 2015
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