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Dietary Sodium Intake is Predicted by Antihypertensive Medication Regimen in Patients With Heart Failure

Smith, Jennifer L. PhD, RN; Lennie, Terry A. PhD, RN, FAHA, FAAN; Chung, Misook L. PhD, RN, FAHA, FAAN; Mudd-Martin, Gia PhD, MPH, RN, FAHA

Journal of Cardiovascular Nursing: July/August 2019 - Volume 34 - Issue 4 - p 313–318
doi: 10.1097/JCN.0000000000000570
Heart Failure
Free

Background Low-sodium diet adherence is foundational to heart failure (HF) self-management. Altered salt taste perception caused by angiotensin-converting enzyme (ACE) inhibitors commonly prescribed to patients with HF may increase sodium consumption. We hypothesized sodium intake, indicated by dietary sodium density, would be significantly higher among patients with HF prescribed ACE inhibitors compared with those not prescribed the drug.

Objective The aim of this study was to assess the association between prescribed ACE inhibitors and dietary sodium density in patients with HF.

Methods We conducted a secondary analysis of baseline data from patients with HF in an observational longitudinal study. Sodium density was derived by dividing averaged daily sodium intake from 4-day food diaries by averaged kilocalories consumed. Medical chart review was conducted to ascertain prescribed medications. Patients were categorized as prescribed and not prescribed an ACE inhibitor. t Tests were conducted to compare sodium intake between groups, and linear regression was conducted to examine whether prescribed ACE inhibitors independently predicted sodium density controlling for age, gender, New York Heart Association class, prescribed diuretics, and β-blockers.

Results Analyses included 255 patients with HF aged 61 ± 12 years, with 67% male, 44% New York Heart Association class III/IV, and 68% prescribed an ACE inhibitor. Compared with those not prescribed an ACE inhibitor, 13% more sodium per kilocalorie was consumed by patients prescribed an ACE inhibitor. Prescribed ACE inhibitor independently predicted dietary sodium density (β = 0.238, P = .009).

Conclusions Sodium intake was higher among patients prescribed ACE inhibitors. Interventions to assist patients with HF with dietary sodium adherence can be informed by assessing medication regimens.

Jennifer L. Smith, PhD, RN Postdoctoral Fellow, College of Nursing, University of Kentucky, Lexington.

Terry A. Lennie, PhD, RN, FAHA, FAAN Senior Associate Dean and Professor, College of Nursing, University of Kentucky, Lexington.

Misook L. Chung, PhD, RN, FAHA, FAAN Professor, College of Nursing, University of Kentucky, Lexington.

Gia Mudd-Martin, PhD, MPH, RN, FAHA Associate Professor, University of Kentucky, College of Nursing Lexington, Kentucky.

The parent study for this secondary analysis received funding from the following sources: NIH R01 NR 009280, NIH P20 NR 010679, Clarion Health Partners (Indiana), and the GCRC UK: M01 RR02602, Emory: M01 RR0039, and Indiana: M01 RR000750.

The authors have no conflicts of interest to disclose.

Correspondence Jennifer L. Smith, PhD, RN, 2201 Regency Rd, Ste 404, Lexington, KY 40503 (jennifer.smith7@uky.edu).

Online date: March 8, 2019

In patients with heart failure, self-care is pivotal to appropriate management of the condition including adherence to a low-sodium diet.1 Unfortunately, many patients with heart failure do not follow the recommended low-sodium diet, with rates of adherence reported to be as low as 22%.1–9 Patients have identified taste of food as one reason for not adhering to this recommendation.10,11 Most patients report that reducing salt makes food unpalatable and limits the enjoyment of eating, negatively affecting quality of life.10,11

Salt taste sensitivity, defined as the ability of an individual to identify the taste of sodium, is composed of 2 dimensions: recognition and detection.12 Recognition is the minimum amount of salt required to identify sodium in a food; detection is the minimum amount of salt required to detect a change in amount of sodium in a food.12 Salt taste sensitivity is a complex phenomenon that is affected by factors that include neural, chemical, and structural inputs, which can be altered by external factors such as medications, dietary salt intake, or health conditions such as heart failure.12–14

Several medications prescribed to treat cardiovascular disease have been associated with disturbances in salt taste sensitivity, as well as other taste disturbances. For example, diuretics are known to reduce saliva production resulting in dry mouth.15 Because saliva is essential for breaking down food into taste substances, reduced saliva production adversely affects ability to taste food. Calcium channel blockers also adversely affect taste by interfering with the availability of zinc.15 Zinc is a central component of the gustin protein that has a major role in the development and maintenance of fungiform papillae. Reduced availability of zinc may reduce papillae involved in taste.16 Adrenergic receptor antagonists are thought to cause a disturbance in taste due to competition over binding sites with catecholamines, which are neurotransmitters that are involved with taste buds.15 Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs), both commonly used treatments in patients with heart failure, have also been shown to cause taste disturbances. In a randomized, controlled, crossover trial, 7 participants were given either an ACE inhibitor or an ARB and tested for taste ability.17 Angiotensin-converting enzyme inhibitors and ARBs were found to worsen taste ability over placebo. Although underlying mechanisms that cause the taste disturbances are not clear, the investigators theorized that it might be related to alteration of the renin-angiotensin system, with angiotensin II and aldosterone both associated with increased salt appetite.13,17

Given that decreased salt taste sensitivity may result in increased salt consumption,17–20 people with heart failure who are prescribed an ACE inhibitor may be at a greater risk for higher salt consumption than those not prescribed an ACE inhibitor. However, the relationship between ACE inhibitors and salt consumption has not been well studied. Therefore, the purpose of this study was to examine whether prescription of an ACE inhibitor predicted sodium consumption. We hypothesized that sodium consumption (calculated based on amount of sodium consumed per kilocalorie or sodium density), as an indicator of salt preference, would be higher in patients with heart failure who were prescribed ACE inhibitors than in patients who were not prescribed ACE inhibitors.

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Methods

Design

This was a secondary analysis of data from patients with heart failure enrolled in an observational longitudinal study to examine the relationships between body fat mass, body fat distribution, cytokine activity, and nutritional intake.21 Patients were recruited into the study and followed for a period of 1 year. For the purposes of our study, we analyzed data collected at baseline.

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Sample

Data from 255 patients with heart failure were included in this analysis. Patients were recruited from outpatient facilities at 3 large academic healthcare facilities between 2006 and 2009. Two of the facilities were located in the southeastern region of the United States, and one was located in the midwestern region. Inclusion criteria were patients who (1) had a confirmed diagnosis of chronic heart failure, (2) had a New York Heart Association (NYHA) classification of I to IV, (3) were stabilized on medication for 3 months before recruitment, (4) had no history of hospitalization in the 3 months before recruitment, and (5) were able to read and speak English. Patients were excluded if they had (1) valvular heart disease as a cause of the heart failure; (2) a myocardial infarction within the last 3 months; (3) been referred for heart transplant; (4) uncontrolled diabetes mellitus (HbA1c > 8%); (5) an illness associated with systemic inflammation, weight loss, or decreased appetite; or (6) a cognitive impairment that prevented giving informed consent.

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Measurement of Variables

Demographic and clinical data

Participant demographic data including age, gender, race/ethnicity, and smoking status were collected through self-report via a sociodemographic questionnaire. New York Heart Association class and prescribed medications were ascertained by trained research nurses using a structured patient interview. Body mass index was calculated using the standard formula of kilograms per square meter.

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Dietary sodium intake

Nutritional data were collected using food diaries that patients completed for a 4-day period, including 3 weekdays and 1 weekend day. The use of 4-day food diaries is a valid method from which nutrients in the diet, including sodium, can be measured.19,22 Before recording food diaries, patients met with a research assistant in their homes who, using food models and pictures of appropriate portion sizes, instructed the patients how to accurately weigh and record dietary information. Each participant was given an electronic digital scale for accurate recording of portion sizes. At the end of the 4-day food diary collection, patients met with a dietitian who collected missing information, verified serving sizes, and verified food preparation methods. Food diaries were analyzed using the Nutrition Data System for Research software (NDS-R 2007; NRCC, Minneapolis, Minnesota).

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Sodium density

Sodium density was defined as the averaged 4-day sodium intake divided by averaged 4-day kilocalorie intake. This was chosen as the metric for salt consumption because it controls for differences in sodium intake because of differences in amount of food consumed and is a better indicator of patients' preferred saltiness of food. This approach has been used by the US Department of Agriculture and the Centers for Disease Control and Prevention to estimate sodium consumption adjusted for energy consumption because higher sodium intake is often accompanied by higher caloric intake.23,24

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Procedure

Approval for this study was obtained from the institutional review boards at each study site. Patients were recruited from affiliated outpatient clinics after referral from a nurse or physician. After providing written informed consent, patients were visited in their homes by a trained research nurse and instructed how to complete 4-day food diaries. The morning after completing the diaries, patients visited 1 of the 3 clinical research centers, at which time demographic and clinical data were collected. A dietitian also reviewed the food diaries with participants during this visit as a way of validating completion and accuracy of the information provided.

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Data Analysis

Patients were categorized into 2 groups: those who were prescribed ACE inhibitors and those who were not. Differences in demographic and clinical characteristics and in dietary sodium density between the 2 groups were compared using independent t tests or χ2 tests as appropriate. A multivariable linear regression was conducted to determine whether being prescribed ACE inhibitors independently predicted dietary sodium density. In the model, we controlled for age, gender, ethnicity (non-Hispanic whites vs other races), NYHA class (I–IV), smoking status (smokers vs nonsmokers), prescribed β-blockers, prescribed ARBs, and prescribed diuretics. All independent variables were entered into 1 model for analysis. An αof .05 was set a priori.

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Results

Sample Characteristics

Most patients were white man with slightly more than half in NYHA class I/II. Mean body mass index was 29.7 ± 6.8. Diuretics (74.5%), β-blockers (88.6%), and ACE inhibitors (69.8%) were commonly prescribed, but less than a quarter of patients were prescribed an ARB. In our sample, 178 patients were prescribed ACE inhibitors (69.8%). Sample characteristics and comparisons between patients who were and were not prescribed an ACE inhibitor are presented in Table 1. The only significant between-group differences were that a greater number of those prescribed an ACE inhibitor were male and were also prescribed a β-blocker.

TABLE 1

TABLE 1

Comparison of sodium density between those prescribed and not prescribed an ACE inhibitor demonstrated that patients prescribed an ACE inhibitor consumed approximately 13% more sodium per kilocalorie than patients who were not prescribed an ACE inhibitor (1.8 ± 0.55 vs 1.6 ± 0.43 mg of sodium/kcal). In our regression model, prescription of an ACE inhibitor predicted higher sodium density (b = 0.230, t234 = 2.566, P = .011), controlling for age, smoking status, ethnicity, NYHA class, and other prescribed medications (Table 2). No other medications predicted sodium density. Among the controlled variables, only BMI predicted sodium density (b = 0.018, t234 = 3.045, P = .002).

TABLE 2

TABLE 2

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Discussion

In support of our hypothesis, patients who were prescribed an ACE inhibitor had a significantly higher consumption of sodium per kilocalorie compared with those who were not prescribed an ACE inhibitor. In accord with current practice guidelines,25,26 patients with heart failure are commonly prescribed medications including ACE inhibitors in conjunction with a low-sodium diet.25 However, as indicated by the results of our study, prescribed ACE inhibitors may present a barrier to low-sodium diet adherence. Supporting our findings are studies that have shown ACE inhibitors are associated with taste disturbances.12,17,27 Taste disturbances most commonly associated with ACE inhibitors range from loss of taste to alteration of salty, sweet, or metallic tastes that include a lingering taste in the mouth or taste confusions such as sweet for salty or sweet for bitter.28–30 These disturbances may result in lowered salt taste sensitivity and increased salt consumption.19

Other medications are also suspected to produce taste disturbances, such as ARBs, diuretics, and β-blockers.12,17 However, similar to other studies,12 only ACE inhibitors predict dietary sodium density in our patients with heart failure. The effect of ACE inhibitors may be exacerbated by heart failure–induced overactivation of the renin-angiotensin-aldosterone system, which is linked to water and salt consumption behaviors.13 Angiotensin-converting enzyme inhibitors work by preventing the conversion of angiotensin I to angiotensin II and increasing levels of bradykinins. Angiotensin-converting enzyme inhibitors are also known to chelate with serum zinc, which results in depletion of zinc levels.31 It is possible that the depletion of zinc that occurs with the chelating action of ACE inhibitors causes a disturbance in the functioning of gustin, which in turn produces a disturbance in salt taste. The influence of ACE inhibitors on taste may be due to the reduction of serum zinc concentration through this mechanism.31,32

In contrast, ARBs work by selectively blocking angiotensin II from binding to receptors but have not been linked to serum zinc depletion.17,29 This may explain why being prescribed ARBs did not predict dietary sodium density. Although some diuretics have also been linked to salt taste sensitivity alterations, this has only been demonstrated for diuretic medications that are less commonly prescribed today. For example, the potassium-sparing diuretic amiloride, rarely used today among patients with heart failure, is thought to block ion channels in the taste receptor membrane altering the flow of sodium ions.29 In a literature review, Doty and colleagues29 demonstrate that amiloride can alter salt taste intensity and sensitivities. Most patients in our study were prescribed loop diuretics, which have not been associated with salt taste sensitivity, as supported by our findings.

de Souza et al13 report that patients with heart failure may have a greater preference for salt in their food. These authors suggest that, because most patients with heart failure have taken multiple medications for a long period, the medication could affect the palatability of food, although they did not define the length of time or the particular medication.13 Consequently, patients with heart failure taking a medication that reduces the ability to taste the salt in their food12 may need to use more salt to meet their already heightened preference. This behavior, in turn, can increase the risk of heart failure exacerbation. Our results suggest that ACE inhibitors may be one of those medications.

The only other variable in the model that was found to be a significant predictor of sodium density in the diet was body mass index. This is not a surprising finding because sodium has been linked to body mass index previously. In particular, excessive sodium consumption has been associated with high-calorie foods and the consumption of sugar-sweetened beverages, which can lead to becoming overweight or obese.33,34 Specifically, sodium consumption in patients with heart failure has been linked to fluid retention, which in turn has been shown to result in increased weight.35 Our results confirm these previously reported associations between body mass index and sodium consumption.33–35

Our finding that gender was not a significant predictor of sodium density may seem to be contrary to findings from previous studies in which men were shown to have higher rates of nonadherence to a low-sodium diet.6 However, because the amount of sodium consumed is tied to the amount of food consumed, using sodium density instead of total sodium intake controlled for differences in amount of food consumed between men and women. Consequently, this method allowed us to directly compare preferred level of sodium in food between men and women.

A limitation of our study was that we did not use a measure of medication adherence. Rather, patients reported a list of which medications they were taking during the structured patient interviews. It is unknown whether a certain level of adherence to ACE inhibitors is necessary for ACE inhibitor use to be associated with sodium density. Further research is required to further explore this link. Another limitation was that there was not an objective measure of salt taste function such as salt taste sensitivity. Although the addition of such a measure would provide more specific data about taste, sodium density is a proxy for sodium consumption and supports conclusions about taste function based on eating behavior.

The findings from our study can inform educational efforts performed by nurses interacting with patients with heart failure. Understanding that ACE inhibitor use is associated with an increase in sodium consumption per kilocalorie, possibly because of alteration in salt taste sensitivity, will allow providers to preemptively plan for this side effect. Nurses can educate patients who are taking ACE inhibitors regarding the expected decrease in salt taste sensitivity. To offset this effect, nurses can also emphasize means by which the taste of food can be enhanced such as exploring the use of spices that can enhance flavor without increasing the use of salt. Involving a trained dietitian on the care team could be of a particular benefit for patients who are prescribed ACE inhibitors. In addition, some researchers have shown that prescribing zinc with ACE inhibitors may decrease the drug's influence on salt taste sensitivity.31 The reason for this may be due to an effect of ACE inhibitors that is thought to alter zinc at the receptor level, which changes the conversion of angiotensin I to angiotensin II. This is because zinc is necessary for the catalytic action of ACE.13,29,36 In addition, taste disturbance is linked to zinc deficiency, which may explain why this drug produces the effect.12,27,31,37 Future research efforts should explore the use of zinc supplements to offset this effect. Likewise, when educating patients with heart failure, consideration of possible taste disturbances may allow nurses to be more specific when discussing changes in taste that may present a barrier when patients attempt to alter their diets. Nurses may be able to offer advice on how to acclimate to decreased sodium in the diet while also dealing with a possible decrease in taste sensitivity, suggesting seasoning substitutes that will enhance the flavor of food without raising sodium content. More research is required to further refine information regarding the association of ACE inhibitor use and sodium consumption as well as to develop educational interventions aimed at helping those on ACE inhibitors to decrease their sodium consumption. Authors of future research should include measures of salt taste sensitivity to further elucidate the effects of ACE inhibitor use on taste perception.

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Conclusions

The finding that prescribed ACE inhibitors predicted the sodium consumption of patients with heart failure has implications for interventions to improve heart failure self-care. When aware of the potential alteration of sodium consumption associated with ACE inhibitors, nurses and other health professionals can closely monitor dietary sodium intake of patients prescribed ACE inhibitors and provide appropriate education and interventions. These measures can better support adherence to low-sodium diet recommendations among patients with heart failure, thereby decreasing the risk of heart failure exacerbation and rehospitalization.

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What’s New and Important

  • ACE inhibitor prescription status predicted sodium consumption in patients with heart failure.
  • Patients prescribed ACE inhibitors consumed approximately 13% more sodium than those who were not prescribed ACE inhibitors.
  • This information can inform more effective educational interventions to help patients prescribed ACE inhibitors to lower their sodium consumption.
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REFERENCES

1. Riegel B, Moser DK, Anker SD, et al. State of the science: promoting self-care in persons with heart failure: a scientific statement from the American Heart Association. Circulation. 2009;120(12):1141–1163.
2. Arcand J, Ivanov J, Sasson A, et al. A high-sodium diet is associated with acute decompensated heart failure in ambulatory heart failure patients: a prospective follow-up study. Am J Clin Nutr. 2011;93(2):332–337.
3. Bui AL, Horwich TB, Fonarow GC. Epidemiology and risk profile of heart failure. Nat Rev Cardiol. 2011;8(1):30–41.
4. Chung ML, Lennie TA, de Jong M, Wu JR, Riegel B, Moser DK. Patients differ in their ability to self-monitor adherence to a low-sodium diet versus medication. J Card Fail. 2008;14(2):114–120.
5. Chung ML, Lennie TA, Mudd-Martin G, Moser DK. Adherence to a low-sodium diet in patients with heart failure is best when family members also follow the diet: a multicenter observational study. J Cardiovasc Nurs. 2015;30(1):44–50.
6. Chung ML, Moser DK, Lennie TA, et al. Gender differences in adherence to the sodium-restricted diet in patients with heart failure. J Card Fail. 2006;12(8):628–634.
7. Colin-Ramirez E, Woo E, Wong N, Ezekowitz JA. Association between self-reported adherence to a low-sodium diet and dietary habits related to sodium intake in heart failure patients. J Cardiovasc Nurs. 2015;30(1):58–65.
8. Lennie TA, Worrall-Carter L, Hammash M, et al. Relationship of heart failure patients' knowledge, perceived barriers, and attitudes regarding low-sodium diet recommendations to adherence. Prog Cardiovasc Nurs. 2008;23(1):6–11.
9. Lennie TA, Song EK, Wu JR, et al. Three gram sodium intake is associated with longer event-free survival only in patients with advanced heart failure. J Card Fail. 2011;17(4):325–330.
10. Bentley B, De Jong MJ, Moser DK, Peden AR. Factors related to nonadherence to low sodium diet recommendations in heart failure patients. Eur J Cardiovasc Nurs. 2005;4(4):331–336.
11. Heo S, Lennie TA, Moser DK, Okoli C. Heart failure patients' perceptions on nutrition and dietary adherence. Eur J Cardiovasc Nurs. 2009;8(5):323–328.
12. Wessler JD, Hummel SL, Maurer MS. Dietary interventions for heart failure in older adults: re-emergence of the hedonic shift. Prog Cardiovasc Dis. 2014;57(2):160–167.
13. de Souza JT, Matsubara LS, Menani JV, Matsubara BB, Johnson AK, De Gobbi JI. Higher salt preference in heart failure patients. Appetite. 2012;58(1):418–423.
14. Shigemura N, Iwata S, Yasumatsu K, et al. Angiotensin II modulates salty and sweet taste sensitivities. J Neurosci. 2013;33(15):6267–6277.
15. Roura E, Foster S, Winklebach A, et al. Taste and hypertension in humans: targeting cardiovascular disease. Curr Pharm Des. 2016;22:2290–2305.
16. Henkin RI. Zinc in taste function : a critical review. Biol Trace Elem Res. 1984;6(3):263–280.
17. Tsuruoka S, Wakaumi M, Araki N, Ioka T, Sugimoto K, Fujimura A. Comparative study of taste disturbance by losartan and perindopril in healthy volunteers. J Clin Pharmacol. 2005;45(11):1319–1323.
18. Rabin M, Poli de Figueiredo CE, Wagner MB, Antonello ICF. Salt taste sensitivity threshold and exercise-induced hypertension. Appetite. 2009;52(3):609–613.
19. Piovesana Pde M, Sampaio Kde L, Gallani MC. Association between taste sensitivity and self-reported and objective measures of salt intake among hypertensive and normotensive individuals. ISRN Nutr. 2012;2013:301213.
20. Michikawa T, Nishiwaki Y, Okamura T, Asakura K, Nakano M, Takebayashi T. The taste of salt measured by a simple test and blood pressure in Japanese women and men. Hypertens Res. 2009;32:399–403.
21. Lennie TA, Andreae C, Rayens MK, et al. Micronutrient deficiency independently predicts time to event in patients with heart failure. J Am Heart Assoc. 2018;7(17):e007251.
22. Bentley B. A review of methods to measure dietary sodium intake. J Cardiovasc Nurs. 2006;21(1):63–67.
23. Carriquiry A, Moshfegh AJ, Steinfeldt LC, et al. Trends in the prevalence of excess dietary sodium intake—United States, 2003–2010. Morb Mortal Wkly Rep. 2013; https://www.cdc.gov/mmwr/preview/mmwrhtml/mm6250a1.htm. Accessed October 4, 2018.
24. Guenther PM, Lyon JM, Appel LJ. Modeling dietary patterns to assess sodium recommendations for nutrient adequacy. Am J Clin Nutr. 2013;97(4):842–847.
26. Writing Committee Members; Yancy CW, Jessup M, et al. 2016 ACC/AHA/HFSA Focused update on new pharmacological therapy for heart failure: an update of the 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association task force on clinical practice guidelines and the Heart Failure Society of America. Circulation. 2016;134(13):e282–e293.
27. Golik A, Zaidenstein R, Dishi V, et al. Effects of captopril and enalapril on zinc metabolism in hypertensive patients. J Am Coll Nutr. 1998;17(1):75–78.
28. Neil-Dwyer G, Marus A. ACE inhibitors in hypertension: assessment of taste and smell function in clinical trials. J Hum Hypertens. 1989;3(suppl 1):169–176.
29. Doty RL, Philip S, Reddy K, Kerr KL. Influences of antihypertensive and antihyperlipidemic drugs on the senses of taste and smell: a review. J Hypertens. 2003;21(10):1805–1813.
30. McNeill JJ, Anderson A, Christophidis N, Jarrott B, Louis WJ. Taste loss associated with captopril treatment. Br Med J. 1979;2(6204):1555–1556.
31. Takaoka T, Sarukura N, Ueda C, et al. Effects of zinc supplementation on serum zinc concentration and ratio of apo/holo-activities of angiotensin converting enzyme in patients with taste impairment. Auris Nasus Larynx. 2010;37(2):190–194.
32. Tsuruoka S, Wakaumi M, Ioka T, et al. Angiotensin II receptor blocker-induces blunted taste sensitivity: comparison of candesartan and valsartan. Br J Clin Pharmacol. 2005;60(2):204–207.
33. Nam GE, Kim SM, Choi MK, et al. Association between 24-h urinary sodium excretion and obesity in Korean adults: a multicenter study. Nutrition. 2017;41:113–119.
34. Song HJ, Cho YG, Lee HJ. Dietary sodium intake and prevalence of overweight in adults. Metabolism. 2013;62(5):703–708.
35. He FJ, Burnier M, Macgregor GA. Nutrition in cardiovascular disease: salt in hypertension and heart failure. Eur Heart J. 2011;32(24):3073–3080.
36. Bünning P, Riordan JF. The functional role of zinc in angiotensin converting enzyme: implications for the enzyme mechanism. J Inorg Biochem. 1985;24(3):183–198.
37. Noh H, Paik HY, Kim J, Chung J. Salty taste acuity is affected by the joint action of αENaC A663T gene polymorphism and available zinc intake in young women. Nutrients. 2013;5(12):4950–4963.
Keywords:

ACE inhibitor; heart failure; salt taste; sodium consumption; sodium density

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