International Journal of Cardiology 176 (2014) 1023–1024

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Letter to the Editor

Albumin may prevent hypertension by inhibiting renin angiotensin aldosterone system Eiji Oda ⁎ Medical Check-up Center, Tachikawa Medical Center, Nagachou 2-2-16, Nagaoka, Niigata, 940-0053, Japan

a r t i c l e

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Article history: Received 9 May 2014 Accepted 24 July 2014 Available online 1 August 2014 Keywords: Albumin Hypertension Angiotensin converting enzyme Aldosterone

Dear Editor, Decreased serum albumin concentrations predicted hypertension in a Japanese health screening population comprised of 1385 normotensive men and 855 normotensive women without cardiovascular disease at baseline (1). Compared with the lowest quartile of serum albumin (Q1) (3.0–4.1 g/dL), the multivariable adjusted hazard ratios (95% confidence intervals; p values) of hypertension for the second (Q2) (4.2– 4.3 g/dL), third (Q3) (4.4 g/dL) and fourth (Q4) (4.5–5.0 g/dL) quartiles of serum albumin were 0.765 (0.574–1.018; p = 0.066), 0.628 (0.440– 0.895; p = 0.010) and 0.520 (0.364–0.742; p b 0.001), respectively (Table 1). However, contrary to the future blood pressure, the crosssectional blood pressure was rather positively correlated with the concentrations of serum albumin (1). The cross-sectional positive association between the serum albumin level and blood pressure may be due to an increase in vascular volume caused by an increase in the osmotic pressure connected with an increase in serum albumin concentrations. However, the underlying mechanisms that albumin may prevent hypertension are unknown. Recently, Fagyas et al. reported that serum albumin is a potent physiological inhibitor of angiotensin converting enzyme (ACE), and the enzymatic activity of intravascular ACE appears to be almost completely suppressed by serum albumin when it is present at physiological concentrations (2). Fagyas et al. are not the first to identify serum albumin as an endogenous inhibitor of ACE. Klauser et al. identified serum albumin as an endogenous inhibitor of ACE in

1979 (3). It has been reported that the postoperative infusion of serum albumin frequently evokes hypotension in patients receiving ACE inhibitor therapy (4). The physiological serum albumin concentrations are several times higher (3.5–5.2 g/dL) than the half maximal ACE inhibitory concentrations for albumin (0.57–0.98 g/dL), suggesting the complete suppression of intravascular ACE activity by serum albumin in vivo (2). Moreover, they tested ACE inhibition by albumin on human sera and human blood vessels and suggested that the ACE activity is significantly suppressed as long as the albumin concentration is at least 3.0 g/dL. They hypothesized that serum albumin does not inhibit all forms of ACE equally. According to this hypothesis, ACE has a lower affinity for albumin in some tissues or has a higher local concentration than that in the serum. Albumin-mediated inhibition is therefore limited in these locations, while ACE inhibitor drugs can potently inhibit these enzymes. Under these conditions, albumin may inhibit the local ACE activity to some degree, but it can be even further inhibited by ACE inhibitor drugs (2). Intravascular ACE may be completely inhibited by serum albumin in its physiological concentrations while tissue ACEs, such as renal, adrenal, cardiac and adipose tissue ACE, may be partially inhibited by tissue albumin in proportion to the tissue concentration of albumin which may be parallel to the serum concentration of albumin. Among tissue ACEs, adrenal ACE may play an important role in the pathogenesis of hypertension through the secretion of aldosterone. A decreased inhibition of adrenal ACE may result in an increased secretion of aldosterone which plays a central role in the regulation of blood pressure mainly by acting on the distal tubules and collecting ducts of the nephron, increasing reabsorption of ions and water in the kidney, to cause the conservation of sodium, secretion of potassium, increased water retention, and increased blood pressure. Using the above mentioned study data (1), the author investigated the relationship between serum albumin and potassium. The Pearson's correlation coefficients (p values) between serum albumin and potassium and sodium were 0.129 (b0.001) and 0.026 (0.215), respectively and the mean (SD) of potassium in Q1, Q2, Q3 and Q4 of serum albumin was 4.26 (0.28) mEq/L, 4.33 (0.32) mEq/L, 4.35 (0.32) mEq/L and 4.39 (0.36) mEq/L, respectively (Table 1). These positive associations between serum albumin and potassium concentrations suggest an inverse association between serum albumin and aldosterone. Therefore, albumin may prevent hypertension by inhibiting renin angiotensin aldosterone system. Conflict of interest

⁎ Tel.: +81 258 36 6221; fax: +81 258 34 1113. E-mail address: [email protected].

http://dx.doi.org/10.1016/j.ijcard.2014.07.078 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.

The author has no conflict of interest.

1024

E. Oda / International Journal of Cardiology 176 (2014) 1023–1024

Table 1 Potassium concentration and incidence and hazard ratio of hypertension by the quartile of serum albumin. Q1 n Albumin g/dL Potassium mEq/La Incidence %/year Hazard ratiob (95% CIc) p a

Q2

Q3

Q4

543 795 3.0–4.1 4.2–4.3 4.26 (0.28) 4.33 (0.32)

372 4.4–4.4 4.35 (0.32)

530 4.5–5.0 4.39 (0.36)

4.6

3.5

3.7

3.1

1

0.77 (0.57–1.02) 0.63 (0.44–0.90) 0.52 (0.36–0.74) 0.066

0.010

b0.001

Mean (SD). b Adjusted for current smoking, daily alcohol drinking, body mass index, proteinuria, estimated glomerular filtration rate, uric acid, fasting glucose, log triglycerides, log high-sensitivity C-reactive protein, white blood cells, hemoglobin and systolic blood pressure. c Confidence interval.

Acknowledgements and disclosures The author received no financial support and declares no conflict of interest. References [1] Oda E. Decreased serum albumin predicts hypertension in a Japanese health screening population. Intern Med 2014;53:655–60. [2] Fagyas M, Uri K, Siket IM, et al. New Perspectives in the Renin–Angiotensin–Aldosterone System (RAAS) II: albumin suppresses angiotensin converting enzyme (ACE) activity in human. PLoS One 2014;9:e87844. [3] Klauser RJ, Robinson CJ, Marinkovic DV, Erdös EG. Inhibition of human peptidyl dipeptidase (angiotensin I converting enzyme: kininase II) by human serum albumin and its fragments. Hypertension 1979;1:281–6. [4] Howard G, Downward G, Bowie D. Human serum albumin induced hypotension in the postoperative phase of cardiac surgery. Anaesth Intensive Care 2001;29:591–4.

Albumin may prevent hypertension by inhibiting renin angiotensin aldosterone system.

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