Antihypertensive treatment in diabetes and diuretics

Česká verzia

Authors: P. Bouček
Authors place of work: Centrum diabetologie IKEM, Praha, přednosta prof. MUDr. Terezie Pelikánová, DrSc.
Published in the journal: Vnitř Lék 2005; 51(6): 728-723
Category: Reviews

Summary

Blood pressure elevation occurs more commonly among diabetic patients than in non–diabetic subjects and represents one of the main reasons for their high cardiovascular risk. Sodium retention is an important pathogenic factor contributing to the genesis of hypertension in diabetes. Effective blood pressure reduction in diabetic patients, for which combination drug therapy is generally needed from the outset, confers an exceptionally high benefit with regard to vascular and renal outcomes. Thiazide diuretics are not recommended as optimal first-line treatment in hypertensive diabetic patients since they may be associated with adverse metabolic effects. However, due to their effect on sodium excretion they represent a very useful component of drug combination therapy. When used with ACE inhibitors or AT₁-blockers, thiazide diuretics may help to attain the low target levels of current treatment guidelines, especially with regard to systolic blood pressure. Adequate doses of loop diuretics are needed for the maintenance of a balanced sodium and water metabolism in advanced stages of diabetic nephropathy.

Key words:
diabetes mellitus – hypertension – diuretics

Zdroje

1. 2003 European Society of Hypertension–European Society of Cardiology guidelines for the management of arterial hypertension. J Hypertens 2003; 21: 1011–1053.

2. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. JAMA 2003; 289: 2560–2572.

3. ALLHATT. Major outcomes in highrisk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic. JAMA 2002; 288: 2981–2997.

4. UKPDS. Tight blood pressure control and risk of macrovascular complications in type 2 diabetes. Brit Med J 1998; 317: 703–713.

5. Amery A, Berthoux P, Bulpitt CJ et al. Glucose intolerance during diuretic therapy. Results of trial by the European Working Party on Hypertension in the Elderly. Lancet 1978; 1: 681–683.

6. Ames RP The effect of antihypertensive drugs on serum lipids and lipoproteins. I. Diuretics. Drugs 1986; 32: 260–278.

7. Barnett A, Dodson PM. Hypertension and diabetes. 3. ed. London: Science Press 2000.

8. Brenner BM, Cooper ME, de Zeeuw D et al. Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. N Engl J Med 2001; 345: 861–869.

9. Cífková R, Horký K, Widimský J sr et al. Doporučení České společnosti pro hypertenzi. Doporučení diagnostických a léčebných postupů u arteriální hypertenze – verze 2004. http://www.hypertension.cz

10. Colhoun HM, Dong W, Barakatt MT et al. The scope for cardiovascular disease risk factor intervention among people with diabetes mellitus in England: A population-based analysis from the Health Surveys for England 1991–94. Diabet Med 1999; 16: 35–40.

11. Curb JD, Pressel SL, Cutler JA et al. Effect of diuretic-based antihypertensive treatment on cardiovascular disease risk in older diabetic patients with isolated systolic hypertension. Systolic Hypertension in the Elderly Program Cooperative Research Group. JAMA 1996; 276: 1886–1892.

12. Dillon JJ. The quantitative relationship between treated blood pressure and progression of diabetic renal disease. Am J Kidney Dis 1993; 22: 798–802.

13. DiPetrillo K, Coutermarsh B, Soucy N et al. Tumor necrosis factor induces sodium retention in diabetic rats through sequential effects on distal tubule cells. Kidney Int 2004; 65: 1676–1683.

14. Dornhorst A, Powell SH, Pensky J. Aggravation by propranolol of hyperglycaemic effect of hydrochlorothiazide in type II diabetics without alteration of insulin secretion. Lancet 1985; 1: 123–126.

15. Feldt-Rasmussen B, Mathiesen ER, Deckert T et al. Central role for sodium in the pathogenesis of blood pressure changes independent of angiotensin, aldosterone and catecholamines in Type-1 (insulin-dependent) diabetes mellitus. Diabetologia 1987; 30: 610–617.

16. Fox JC, Leight K, Sutradhar SC et al. The JNC 7 approach compared to conventional treatment in diabetic patients with hypertension: a double-blind trial of initial monotherapy vs. combination therapy. J Clin Hypertens 2004; 6: 437–444.

17. Hansson L, Zanchetti A, Carruthers SG et al. Effects of intensive blood-pressure lowering and low-dose aspirin in patients with hypertension: principal results of the Hypertension Optimal Treatment (HOT) randomised trial. Lancet 1998; 351: 1755–1762.

18. Hannedouche TP, Delgrado AG, Gnoinsahe DA et al. Renal hemodynamics and segmental tubular sodium reabsorption in early type 1 diabetes. Kidney Int 1990; 37: 1126–1133.

19. Heidbreder D, Froer KL, Bauer B et al. Combination of ramipril and hydrochlorothiazide in the treatment of mild to moderate hypertension – Part 2: An open long-term study of efficacy and safety. Clin Cardiology 1993; 16: 47–52.

20. Helderman JH, Elahi D, Andersen DK et al. Prevention of the glucose intolerance of thiazide diuretics by maintenance of body potassium. Diabetes 1983; 32: 106–111.

21. Kmoch J, Svoboda Z. Thiazidová saluretika a glukózová tolerance u nemocných s hypertenzí. Vnitř Lék 1974; 20: 967–973.

22. Kmoch J, Svoboda Z. Vliv dlouhodobého podávání hydrochlorothiazidu na glycidovou toleranci diabetiků. Vnitř Lék 1975; 21: 980–985.

23. Kostis JB, Wilson AC, Freudenberger RS et al. Long–term effect of diuretic–based therapy on fatal outcomes in subjects with isolated systolic hypertension with and without diabetes. Am J Cardiol 2005; 95: 29–35.

24. Lewis PJ, Kohner EM, Petrie A et al. Deterioration of glucose tolerance in hypertensive patients on prolonged diuretic treatment. Lancet 1976; 1: 564–566.

25. Locatelli F, Canaud, B., Eckhardt H et al. The importance of diabetic nephropathy in current nephrological practice. Nephrol Dial Transplant 2003; 18: 1716–1725.

26. Mogensen CE. Long–term antihypertensive treatment inhibiting progression of diabetic nephropathy. Brit Med J 1982; 285: 685–688.

27. Molinari C, Battaglia A, Bona G et al. Mechanisms of the renal vasodilation caused by insulin in anesthetized pigs. Life Sci 2001; 69: 1699–1708.

28. Pacy P, Dodson PM, Beevers M et al. Prevalence of hypertension in white, black and Asian diabetics in a district hospital diabetic clinic. Diabetic Med 1985; 2: 125–130.

29. Parving HH, Andersen AR, Smidt UM et al. Early aggresive antihypertensive treatment reduces rate of decline in kidney function in diabetic nephropathy. Lancet 1983; 1: 1175–1179.

30. Roland JM, O’Hare JP, Walters G et al. Sodium retention in response to saline infusion in uncomplicated diabetes mellitus. Diabetes Res 1986; 3: 213–215.

31. Rudberg S, Lemne C, Persson B et al. The dopaminergic response to high salt diet in insulin-dependent diabetes mellitus and in family history of hypertension. Pediatric Nephrol 1997; 11: 169–173.

32. Stenvinkel P, Saggar–Malik AK, Wahrenberg H et al. Impaired intrarenal dopamine production following intravenous sodium chloride infusion in Type 1 (insulin-dependent) diabetes mellitus. Diabetologia 1991; 34: 114–118.

33. Stenvinkel P, Bolinder J, Alvestrand A. Effects of insulin on renal haemodynamics and the proximal and distal tubular sodium handling in healthy subjects. Diabetologia 1992; 35: 1042–1048.

34. Stenvinkel P, Ottosson-Seeberger A, Alvestrand A. Renal haemodynamics and sodium handling in moderate renal insufficiency: the role of insulin resistance and dyslipidaemia. J Am Soc Nephrol 1995; 5: 1–10.

35. Tarnow L, Rossing P, Gall MA et al. Prevalence of arterial hypertension in diabetic patients before and after the JNC-V. Diabetes Care 1994; 17: 1247–1251.

36. Trenkwalder P, Ulmer HJ, Weidinger G et al. Efficacy and safety of valsartan 160mg/hydrochlorothiazide 25 mg combination in patients with hypertension not adequately controlled by valsartan 160 mg/hydrochlorothiazide 12.5 mg. Clin Drug Invest 2004; 24: 593–602.

37. Tsuchida H, Imai G, Shima Y et al. Mechanisms of sodium load-induced hypertension in non-insulin dependent diabetes mellitus model rats: defective dopaminergic system to inhibit Na-KATPase

activity in renal epithelial cells. Hypertens Res 2001; 24: 127–135.

38. Turner R, Millns H, Neil HA et al. Risk factors for coronary artery disease in non-insulin dependent diabetes mellitus: United Kingdom Prospective Diabetes Study. Brit Med J 1998; 316: 823–828.

39. Vallon V, Huang DY, Deng A et al. Salt-sensitivity of proximal reabsorption alters macula densa salt and explains the paradoxical effect of dietary salt on glomerular filtration rate in diabetes mellitus. J Am Soc Nephrol 2002; 13: 1865–1871.

40. Verdecchia P, Reboldi G, Angeli F et al. Adverse prognostic significance of new diabetes in treated hypertensive subjects. Hypertension 2004; 43: 963–969.