How long does it take for diuretics to lower blood pressure

High blood pressure is a common health concern. People can reduce their blood pressure in several ways, including diet, exercise, and blood pressure medication.

How long it takes to lower blood pressure depends on different factors, including:

  • how high someone’s blood pressure is at the start
  • what methods they used to lower it
  • other individual health factors

While blood pressure medications work relatively quickly, people usually need to stick to certain changes in their diet and lifestyle to keep their blood pressure down long term.

This article looks at how long it takes to lower blood pressure with different methods.

A doctor diagnosing high blood pressure, or hypertension, may prescribe one or more drugs to help control it and reduce the risk for heart attack and stroke.

These drugs may include diuretics, beta-blockers, and ACE inhibitors, alone or together.

Medication helps lower blood pressure quickly, typically within a few days. However, it may not be the best long-term treatment due to side effects.

Medication can help manage high blood pressure while a person changes their underlying lifestyle that may be causing high blood pressure.

Diet changes can quickly lower blood pressure in many cases.

A study in the journal Hypertension reported that people following the Dietary Approaches to Stop Hypertension (DASH) diet lowered their blood pressure by 1–4 millimeters of mercury (mm Hg) in 1 week.

The same study noted that reducing sodium intake gradually decreased blood pressure over 4 weeks.

Making consistent, long-term changes to diet and lifestyle can help keep blood pressure in a healthy range.

The following sections discuss how to reduce blood pressure using various methods.

A healthful diet can reduce the risk of high blood pressure and can help lower blood pressure. Conversely, certain diets can increase a person’s blood pressure by causing water retention or weight gain.

Diets high in the following components can increase blood pressure:

  • salt or sodium
  • saturated fats
  • trans fats
  • sugars

A healthful diet includes plenty of heart healthy foods, including:

  • fruits
  • vegetables
  • whole grains
  • other fiber-rich foods
  • unsaturated fats

Many doctors will include diet plans as part of treatment for high blood pressure. For instance, the DASH diet plan incorporates heart healthy eating while also reducing foods that increase blood pressure.

Taking steps towards eating a heart healthy diet is a good way to reduce blood pressure. Anyone having trouble changing their diet may want to talk to a dietitian for guidance.

Learn about the best foods for high blood pressure here.

Exercise is an important factor in reducing a person’s blood pressure. Regular exercise helps prevent and reduce high blood pressure.

A review published in the journal Blood Pressure found that regular exercise led to a 3.9% drop in systolic blood pressure and a 4.5% drop in diastolic blood pressure in older adults.

Additionally, exercise has many health benefits and helps control other risk factors for high blood pressure, including overweight and obesity.

Exercise is not a quick fix for high blood pressure but a lifestyle change.

Including regular exercise is one step towards lowering blood pressure and is best when people incorporated it with other factors, such as a healthful diet.

A person’s weight directly influences the heart and circulatory system.

Overweight and obesity increase the risk for high blood pressure and also place extra strain on the heart. For most people, diet and exercise changes are effective ways to manage weight and reduce these risks.

Losing weight in a healthful way that takes time but has many benefits. Learn more here.

High sodium diets increase the risk for issues in the heart, such as high blood pressure. Reducing sodium intake can reduce the risk.

A study published in the Journal of the American College of Cardiology reported that people who reduced their sodium intake lowered their blood pressure by 3–9 mm Hg.

Smoking is a risk factor for a number of heart conditions, along with other effects on the body. It may also influence blood pressure both directly and indirectly.

The American Heart Association (AHA) state that smoking itself increases blood pressure. Every time a person smokes, their blood pressure temporarily goes up.

Additionally, smoking increases the risk of atherosclerosis, which is the buildup of fatty plaque in the arteries.

Atherosclerosis increases a person’s risk for other issues, such as heart attack and stroke. High blood pressure speeds up the process of atherosclerosis.

Quitting smoking can help reduce these risks.

Alcohol is another risk factor for high blood pressure.

A person does not have to eliminate alcohol from their diet in order to benefit. However, reducing alcohol intake can significantly lower blood pressure.

One 2017 study reported that reducing alcohol intake in people who drank more than two drinks per day led to a reduction of 5.5 mm Hg systolic and 4 mm Hg diastolic blood pressure.

Drinking more than two drinks may raise blood pressure.

Stress is another important factor for overall health that may contribute to blood pressure.

An individual’s reaction to stress may influence heart health, as well. For example, some people may turn to alcohol, smoking, or comfort foods. These factors may increase the risk for high blood pressure.

Finding ways to reduce or eliminate stress may help reduce these factors. Stress reductions techniques include:

  • breathing exercises
  • meditation
  • movement activities, such as tai chi or qi gong
  • yoga or gentle stretches
  • other therapies, such as acupuncture or massage
  • removing personal stress triggers

Other heart healthy tips may also help reduce stress, such as getting regular exercise. Stress reduction itself is part of an overall change for heart health.

A number of other factors also increase the risk for high blood pressure, including:

Age and gender also play a role. The AHA note that males under 64 years of age are more likely to have high blood pressure. After 65, females are more likely to have high blood pressure.

Having high blood pressure increases the risk for other serious issues affecting the heart, such as atherosclerosis and heart attack.

Making direct changes to the diet and lifestyle may bring about relatively quick reductions in blood pressure. In some cases, doctors may recommend drugs to help keep the blood pressure in line as an individual makes changes to their diet and lifestyle.

While some changes can produce results quickly, it is important to continue with these trends. Switching to old habits may simply revert these changes and bring the person’s blood pressure back up.

Rather than a quick fix, consistent changes are the best way to reduce blood pressure long-term.

Papers of special note have been highlighted as:

• of interest

•• of considerable interest

1. Lloyd-Jones D, Adams R, Carnethon M, et al. Heart disease and stroke statistics – 2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2009;119(3):480–486. [PubMed] [Google Scholar]

2. Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003;42(6):1206–1252. [PubMed] [Google Scholar]

3. Ellison DH, Velazquez H, Wright FS. Thiazide-sensitive sodium chloride cotransport in early distal tubule. Am J Physiol. 1987;253(3 Pt 2):F546–F554. [PubMed] [Google Scholar]

4. Bachmann S, Velazquez H, Obermuller N, Reilly RF, Moser D, Ellison DH. Expression of the thiazide-sensitive Na–Cl cotransporter by rabbit distal convoluted tubule cells. J Clin Invest. 1995;96(5):2510–2514. [PMC free article] [PubMed] [Google Scholar]

5. Obermuller N, Bernstein P, Velazquez H, et al. Expression of the thiazide-sensitive Na–Cl cotransporter in rat and human kidney. Am J Physiol. 1995;269(6 Pt 2):F900–F910. [PubMed] [Google Scholar]

6. Adrogue HJ, Madias NE. Sodium and potassium in the pathogenesis of hypertension. N Engl J Med. 2007;356(19):1966–1978. [PubMed] [Google Scholar]

7. Conway J, Lauwers P. Hemodynamic and hypotensive effects of long-term therapy with chlorothiazide. Circulation. 1960;21:21–27. [PubMed] [Google Scholar]

8. van Brummelen P, Man in ‘t Veld AJ, Schalekamp MA. Hemodynamic changes during long-term thiazide treatment of essential hypertension in responders and nonresponders. Clin Pharmacol Ther. 1980;27(3):328–336. [PubMed] [Google Scholar]

9. Lake CR, Ziegler MG, Coleman MD, Kopin IJ. Hydrochlorothiazide-induced sympathetic hyperactivity in hypertensive patients. Clin Pharmacol Ther. 1979;26(4):428–432. [PubMed] [Google Scholar]

10. Wilson IM, Freis ED. Relationship between plasma and extracellular fluid volume depletion and the antihypertensive effect of chlorothiazide. Circulation. 1959;20:1028–1036. [PubMed] [Google Scholar]

11. Tarazi RC, Dustan HP, Frohlich ED. Long-term thiazide therapy in essential hypertension. Evidence for persistent alteration in plasma volume and renin activity. Circulation. 1970;41(4):709–717. [PubMed] [Google Scholar]

12. Winer BM. The antihypertensive actions of benzothiadiazines. Circulation. 1961;23:211–218. [PubMed] [Google Scholar]

13. Anderson J, Godfrey BE, Hill DM, Munro-Faure AD, Sheldon J. A comparison of the effects of hydrochlorothiazide and of frusemide in the treatment of hypertensive patients. Q J Med. 1971;40(160):541–560. [PubMed] [Google Scholar]

14. Holland OB, Gomez-Sanchez CE, Kuhnert LV, Poindexter C, Pak CY. Antihypertensive comparison of furosemide with hydrochlorothiazide for black patients. Arch Intern Med. 1979;139(9):1015–1021. [PubMed] [Google Scholar]

15•. Hughes AD. How do thiazide and thiazide-like diuretics lower blood pressure? J Renin Angiotensin Aldosterone Syst. 2004;5(4):155–160. Comprehensive review of thiazide blood pressure-lowering mechanisms. [PubMed] [Google Scholar]

16. Shah S, Khatri I, Freis ED. Mechanism of antihypertensive effect of thiazide diuretics. Am Heart J. 1978;95(5):611–618. [PubMed] [Google Scholar]

17. Aleksandrow D, Wysznacka W, Gajewski J. Influence of chlorothiazide upon arterial responsiveness to nor-epinephrine in hypertensive subjects. N Engl J Med. 1959;261:1052–1055. [PubMed] [Google Scholar]

18. Freis ED, Wanko A, Schnaper HW, Frohlich ED. Mechanism of the altered blood pressure responsiveness produced by chlorothiazide. J Clin Invest. 1960;39:1277–1281. [PMC free article] [PubMed] [Google Scholar]

19. Colas B, Slama M, Collin T, Safar M, Andrejak M. Mechanisms of methyclothiazide-induced inhibition of contractile responses in rat aorta. Eur J Pharmacol. 2000;408(1):63–67. [PubMed] [Google Scholar]

20. Calder JA, Schachter M, Sever PS. Direct vascular actions of hydrochlorothiazide and indapamide in isolated small vessels. Eur J Pharmacol. 1992;220(1):19–26. [PubMed] [Google Scholar]

21. Calder JA, Schachter M, Sever PS. Potassium channel opening properties of thiazide diuretics in isolated guinea pig resistance arteries. J Cardiovasc Pharmacol. 1994;24(1):158–164. [PubMed] [Google Scholar]

22•. Pickkers P, Hughes AD, Russel FG, Thien T, Smits P. Thiazide-induced vasodilation in humans is mediated by potassium channel activation. Hypertension. 1998;32(6):1071–1076. Studies local direct vasodilation in humans, and calcium-activated potassium channels are implicated as a mechanism. [PubMed] [Google Scholar]

23. Beermann B, Groschinsky-Grind M. Pharmacokinetics of hydrochlorothiazide in man. Eur J Clin Pharmacol. 1977;12(4):297–303. [PubMed] [Google Scholar]

24. Niemeyer C, Hasenfuss G, Wais U, Knauf H, Schafer-Korting M, Mutschler E. Pharmacokinetics of hydrochlorothiazide in relation to renal function. Eur J Clin Pharmacol. 1983;24(5):661–665. [PubMed] [Google Scholar]

25. Kreeft JH, Langlois S, Ogilvie RI. Comparative trial of indapamide and hydrochlorothiazide in essential hypertension, with forearm plethysmography. J Cardiovasc Pharmacol. 1984;6(4):622–626. [PubMed] [Google Scholar]

26. Pickkers P, Russel FG, Hughes AD, Thien T, Smits P. Hydrochlorothiazide exerts no direct vasoactivity in the human forearm. J Hypertens. 1995;13(12 Pt 2):1833–1836. [PubMed] [Google Scholar]

27. Pickkers P, Garcha RS, Schachter M, Smits P, Hughes AD. Inhibition of carbonic anhydrase accounts for the direct vascular effects of hydrochlorothiazide. Hypertension. 1999;33(4):1043–1048. [PubMed] [Google Scholar]

28. Mironneau J, Savineau JP, Mironneau C. Compared effects of indapamide, hydrochlorothiazide and chlorthalidone on electrical and mechanical activities in vascular smooth muscle. Eur J Pharmacol. 1981;75(2–3):109–113. [PubMed] [Google Scholar]

29. Del Rio M, Chulia T, Gonzalez P, Tejerina T. Effects of indapamide on contractile responses and 45Ca2+ movements in various isolated blood vessels. Eur J Pharmacol. 1993;250(1):133–139. [PubMed] [Google Scholar]

30. Abrahams Z, Tan LL, Pang MY, Abrahams B, Tan MM, Wright JM. Demonstration of an in vitro direct vascular relaxant effect of diuretics in the presence of plasma. J Hypertens. 1996;14(3):381–388. [PubMed] [Google Scholar]

31. Abrahams Z, Pang MY, Lam EK, Wright JM. What is the plasma cofactor required by diuretics for direct vascular relaxant effect in vitro? J Hypertens. 1998;16(6):801–809. [PubMed] [Google Scholar]

32. Zhu Z, Zhu S, Liu D, Cao T, Wang L, Tepel M. Thiazide-like diuretics attenuate agonist-induced vasoconstriction by calcium desensitization linked to Rho kinase. Hypertension. 2005;45(2):233–239. [PubMed] [Google Scholar]

33•. Tobian L. Why do thiazide diuretics lower blood pressure in essential hypertension? Annu Rev Pharmacol. 1967;7:399–408. First instance of reverse whole-body regulation theory presented. [PubMed] [Google Scholar]

34. Bennett WM, McDonald WJ, Kuehnel E, Hartnett MN, Porter GA. Do diuretics have antihypertensive properties independent of natriuresis? Clin Pharmacol Ther. 1977;22(5 Pt 1):499–504. [PubMed] [Google Scholar]

35. Roos JC, Boer P, Koomans HA, Geyskes GG, Dorhout Mees EJ. Haemodynamic and hormonal changes during acute and chronic diuretic treatment in essential hypertension. Eur J Clin Pharmacol. 1981;19(2):107–112. [PubMed] [Google Scholar]

36. Roser M, Eibl N, Eisenhaber B, et al. Gitelman syndrome. Hypertension. 2009;53(6):893–897. [PubMed] [Google Scholar]

37. Cruz DN, Simon DB, Nelson-Williams C, et al. Mutations in the Na–Cl cotransporter reduce blood pressure in humans. Hypertension. 2001;37(6):1458–1464. [PubMed] [Google Scholar]

38. Ji W, Foo JN, O’Roak BJ, et al. Rare independent mutations in renal salt handling genes contribute to blood pressure variation. Nat Genet. 2008;40(5):592–599. [PMC free article] [PubMed] [Google Scholar]

39. Calo L, Ceolotto G, Milani M, et al. Abnormalities of Gq-mediated cell signaling in Bartter and Gitelman syndromes. Kidney Int. 2001;60(3):882–889. [PubMed] [Google Scholar]

40. Hebert SC, Mount DB, Gamba G. Molecular physiology of cation-coupled Cl− cotransport: the SLC12 family. Pflugers Arch. 2004;447(5):580–593. [PubMed] [Google Scholar]

41. Maitland-van der Zee AH, Turner ST, Schwartz GL, Chapman AB, Klungel OH, Boerwinkle E. A multilocus approach to the antihypertensive pharmacogenetics of hydrochlorothiazide. Pharmacogenet Genomics. 2005;15(5):287–293. [PubMed] [Google Scholar]

42. Turner ST, Schwartz GL, Chapman AB, Boerwinkle E. WNK1 kinase polymorphism and blood pressure response to a thiazide diuretic. Hypertension. 2005;46(4):758–765. [PubMed] [Google Scholar]

43. Ellison DH, Loffing J. Thiazide effects and adverse effects. Insights from molecular genetics. Hypertension. 2009;54(2):196–202. [PMC free article] [PubMed] [Google Scholar]

44. Moriguchi T, Urushiyama S, Hisamoto N, et al. WNK1 regulates phosphorylation of cation–chloride-coupled cotransporters via the STE20-related kinases, SPAK and OSR1. J Biol Chem. 2005;280(52):42685–42693. [PubMed] [Google Scholar]

45. Wang Y, O’Connell JR, McArdle PF, et al. From the cover: whole-genome association study identifies STK39 as a hypertension susceptibility gene. Proc Natl Acad Sci USA. 2009;106(1):226–231. [PMC free article] [PubMed] [Google Scholar]

46. Richardson C, Rafiqi FH, Karlsson HK, et al. Activation of the thiazide-sensitive Na+–Cl− cotransporter by the WNK-regulated kinases SPAK and OSR1. J Cell Sci. 2008;121(Pt 5):675–684. [PubMed] [Google Scholar]

47. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470–476. [PMC free article] [PubMed] [Google Scholar]

48. Savage PJ, Pressel SL, Curb JD, et al. Influence of long-term, low-dose, diuretic-based, antihypertensive therapy on glucose, lipid, uric acid, and potassium levels in older men and women with isolated systolic hypertension: the Systolic Hypertension in the Elderly Program. SHEP Cooperative Research Group. Arch Intern Med. 1998;158(7):741–751. [PubMed] [Google Scholar]

49••. ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) JAMA. 2002;288(23):2981–2997. Landmark trial that resulted in thiazides being suggested by many guidelines as first-line antihypertensive therapy. [PubMed] [Google Scholar]

50. Lindholm LH, Persson M, Alaupovic P, Carlberg B, Svensson A, Samuelsson O. Metabolic outcome during 1 year in newly detected hypertensives: results of the Antihypertensive Treatment and Lipid Profile in a North of Sweden Efficacy Evaluation (ALPINE study) J Hypertens. 2003;21(8):1563–1574. [PubMed] [Google Scholar]

51•. Elliott WJ, Meyer PM. Incident diabetes in clinical trials of antihypertensive drugs: a network meta-analysis. Lancet. 2007;369(9557):201–207. Meta-analysis of clinical trials showing of all antihypertensives analyzed, β-blockers and thiazide diuretics are associated with the highest risk of diabetes. [PubMed] [Google Scholar]

52. Cooper-Dehoff RM, Wen S, Beitelshees AL, et al. Impact of abdominal obesity on incidence of adverse metabolic effects associated with antihypertensive medications. Hypertension. 2009;55(1):61–68. [PMC free article] [PubMed] [Google Scholar]

53. Pepine CJ, Handberg EM, Cooper-DeHoff RM, et al. A calcium antagonist vs a non-calcium antagonist hypertension treatment strategy for patients with coronary artery disease. The International Verapamil–Trandolapril Study (INVEST): a randomized controlled trial. JAMA. 2003;290(21):2805–2816. [PubMed] [Google Scholar]

54. Barzilay JI, Davis BR, Cutler JA, et al. Fasting glucose levels and incident diabetes mellitus in older nondiabetic adults randomized to receive 3 different classes of antihypertensive treatment: a report from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) Arch Intern Med. 2006;166(20):2191–2201. [PubMed] [Google Scholar]

55. Sica DA. Diuretic-related side effects: development and treatment. J Clin Hypertens (Greenwich) 2004;6(9):532–540. [PMC free article] [PubMed] [Google Scholar]

56. Kasiske BL, Ma JZ, Kalil RS, Louis TA. Effects of antihypertensive therapy on serum lipids. Ann Intern Med. 1995;122(2):133–141. [PubMed] [Google Scholar]

57. Lakshman MR, Reda DJ, Materson BJ, Cushman WC, Freis ED. Diuretics and β-blockers do not have adverse effects at 1 year on plasma lipid and lipoprotein profiles in men with hypertension. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents. Arch Intern Med. 1999;159(6):551–558. [PubMed] [Google Scholar]

58. Williams K, Sniderman AD, Sattar N, D’Agostino R, Jr, Wagenknecht LE, Haffner SM. Comparison of the associations of apolipoprotein B and low-density lipoprotein cholesterol with other cardiovascular risk factors in the Insulin Resistance Atherosclerosis Study (IRAS) Circulation. 2003;108(19):2312–2316. [PubMed] [Google Scholar]

59. Bia MJ, DeFronzo RA. Extrarenal potassium homeostasis. Am J Physiol. 1981;240(4):F257–F268. [PubMed] [Google Scholar]

60. DeFronzo RA, Felig P, Ferrannini E, Wahren J. Effect of graded doses of insulin on splanchnic and peripheral potassium metabolism in man. Am J Physiol. 1980;238(5):E421–E427. [PubMed] [Google Scholar]

61. Sterns RH, Feig PU, Pring M, Guzzo J, Singer I. Disposition of intravenous potassium in anuric man: a kinetic analysis. Kidney Int. 1979;15(6):651–660. [PubMed] [Google Scholar]

62. DeFronzo RA, Sherwin RS, Dillingham M, Hendler R, Tamborlane WV, Felig P. Influence of basal insulin and glucagon secretion on potassium and sodium metabolism. Studies with somatostatin in normal dogs and in normal and diabetic human beings. J Clin Invest. 1978;61(2):472–479. [PMC free article] [PubMed] [Google Scholar]

63. Rowe JW, Tobin JD, Rosa RM, Andres R. Effect of experimental potassium deficiency on glucose and insulin metabolism. Metabolism. 1980;29(6):498–502. [PubMed] [Google Scholar]

64. Choi CS, Thompson CB, Leong PK, McDonough AA, Youn JH. Short-term K(+) deprivation provokes insulin resistance of cellular K(+) uptake revealed with the K(+) clamp. Am J Physiol Renal Physiol. 2001;280(1):F95–F102. [PubMed] [Google Scholar]

65••. Carter BL, Einhorn PT, Brands M, et al. Thiazide-induced dysglycemia: call for research from a working group from the National Heart, Lung, and Blood Institute. Hypertension. 2008;52(1):30–36. National Heart, Lung and Blood Institute calls for research that underlines the importance of further research regarding the mechanism of thiazide-associated dysglycemia. Also a good review of the role of potassium in dysglycemia. [PubMed] [Google Scholar]

66. Knochel JP, Schlein EM. On the mechanism of rhabdomyolysis in potassium depletion. J Clin Invest. 1972;51(7):1750–1758. [PMC free article] [PubMed] [Google Scholar]

67. Agarwal R. Hypertension, hypokalemia, and thiazide-induced diabetes: a 3-way connection. Hypertension. 2008;52(6):1012–1013. [PubMed] [Google Scholar]

68. Pickkers P, Schachter M, Hughes AD, Feher MD, Sever PS. Thiazide-induced hyperglycaemia: a role for calcium-activated potassium channels? Diabetologia. 1996;39(7):861–864. [PubMed] [Google Scholar]

69. Sandstrom PE. Inhibition by hydrochlorothiazide of insulin release and calcium influx in mouse pancreatic β-cells. Br J Pharmacol. 1993;110(4):1359–1362. [PMC free article] [PubMed] [Google Scholar]

70•. Zillich AJ, Garg J, Basu S, Bakris GL, Carter BL. Thiazide diuretics, potassium, and the development of diabetes: a quantitative review. Hypertension. 2006;48(2):219–224. Meta-analysis of clinical trials associating thiazide-induced hypokalemia with hyperglycemia and attenuation of hyperglycemia with potassium treatment. [PubMed] [Google Scholar]

71. Shafi T, Appel LJ, Miller ER, 3rd, Klag MJ, Parekh RS. Changes in serum potassium mediate thiazide-induced diabetes. Hypertension. 2008;52(6):1022–1029. [PMC free article] [PubMed] [Google Scholar]

72••. Smith SM, Anderson SD, Wen S, et al. Lack of correlation between thiazide-induced hyperglycemia and hypokalemia: subgroup analysis of results from the Pharmacogenomic Evaluation of Antihypertensive Responses (PEAR) study. Pharmacotherapy. 2009;29(10):1157–1165. Prospective clinical trial that contrasts with the previous belief that thiazide-induced serum potassium decreases are correlated with hyperglycemia. [PMC free article] [PubMed] [Google Scholar]

73. Ayvaz G, Balos Törüner F, Karakoç A, Yetkin I, Cakir N, Arslan M. Acute and chronic effects of different concentrations of free fatty acids on the insulin secreting function of islets. Diabetes Metab. 2002;28(6 Pt 2):3S7–3S12. [PubMed] [Google Scholar]

74••. Eriksson JW, Jansson PA, Carlberg B, et al. Hydrochlorothiazide, but not candesartan, aggravates insulin resistance and causes visceral and hepatic fat accumulation: the Mechanisms For the Diabetes Preventing Effect of Candesartan (MEDICA) Study. Hypertension. 2008;52(6):1030–1037. Clinical evidence associating visceral fat with thiazide-induced insulin resistance. [PubMed] [Google Scholar]

75•. Reungjui S, Roncal CA, Mu W, et al. Thiazide diuretics exacerbate fructose-induced metabolic syndrome. J Am Soc Nephrol. 2007;18(10):2724–2731. Shows an improvement of thiazide-induced insulin resistance by correcting hyperuricemia or hypokalemia in rats. [PubMed] [Google Scholar]

76. Tikellis C, Cooper ME, Thomas MC. Role of the renin–angiotensin system in the endocrine pancreas: implications for the development of diabetes. Int J Biochem Cell Biol. 2006;38(5–6):737–751. [PubMed] [Google Scholar]

77. Tham DM, Martin-McNulty B, Wang YX, et al. Angiotensin II is associated with activation of NF-κB-mediated genes and downregulation of PPARs. Physiol Genomics. 2002;11(1):21–30. [PubMed] [Google Scholar]

78. Hadchouel J, Delaloy C, Faure S, Achard JM, Jeunemaitre X. Familial hyperkalemic hypertension. J Am Soc Nephrol. 2006;17(1):208–217. [PubMed] [Google Scholar]

79. Mayan H, Vered I, Mouallem M, Tzadok-Witkon M, Pauzner R, Farfel Z. Pseudohypoaldosteronism type II: marked sensitivity to thiazides, hypercalciuria, normomagnesemia, and low bone mineral density. J Clin Endocrinol Metab. 2002;87(7):3248–3254. [PubMed] [Google Scholar]

80. Maitland-van der Zee AH, Turner ST, Schwartz GL, Chapman AB, Klungel OH, Boerwinkle E. Demographic, environmental, and genetic predictors of metabolic side effects of hydrochlorothiazide treatment in hypertensive subjects. Am J Hypertens. 2005;18(8):1077–1083. [PubMed] [Google Scholar]

81. Bozkurt O, de Boer A, Grobbee DE, et al. Variation in renin–angiotensin system and salt-sensitivity genes and the risk of diabetes mellitus associated with the use of thiazide diuretics. Am J Hypertens. 2009;22(5):545–551. [PubMed] [Google Scholar]

82. Carter BL, Ernst ME, Cohen JD. Hydrochlorothiazide versus chlorthalidone: evidence supporting their interchangeability. Hypertension. 2004;43(1):4–9. [PubMed] [Google Scholar]

83. Chanock SJ, Manolio T, Boehnke M, et al. Replicating genotype–phenotype associations. Nature. 2007;447(7145):655–660. [PubMed] [Google Scholar]

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Theoretical mechanisms of thiazide-induced chronic blood pressure lowering

eNOS: Endothelial nitric oxide synthase; KCA: Calcium-activated potassium; TPR: Total peripheral resistance.

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