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Metabolic parameters after changing from hydrochlorothiazide to verapamil treatment in hypertension

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Summary

The effect of verapamil on different metabolic parameters has been studied after changing the treatment of hypertension from hydrochlorothiazide to verapamil monotherapy. Verapamil 80 to 160 mg b.i.d. was continued for 6 months. The antihypertensive efficacy of verapamil was comparable to that of hydrochlorothiazide. Plasma total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides and free fatty acids did not change significantly after the change in treatment; serum total cholesterol, LDL-cholesterol and HDL-cholesterol were 7.28±1.80 (m±SD), 5.11±1.59 and 1.65±0.39 mmol/l at the end of the hydrochlorothiazide period and 7.10±1.92, 5.09±1.70 and 1.56±0.35 mmol/l at the end of the verapamil period, respectively. The only statistically significant differences were the increases in total and LDL-cholesterol after three months on verapamil as compared to the basal values before diuretic therapy. Marked changes were not observed in fasting blood glucose, insulin or C-peptide values. Serum uric acid concentration decreased significantly (p<0.001) from 326±66 to 252±53 mmol/l, and serum potassium level increased significantly (p<0.01) from 3.5±0.4 to 3.9±0.3 mmol/l, on verapamil as compared to the diuretic period. Serum calcium decreased from 2.45±0.10 to 2.37±0.08 mmol/l (p<0.01) and calcium excretion increased significantly (p<0.01) to 5.43±2.55 mmol/24 h during verapamil administration from the level of 3.56±2.78 mmol/24 h whilst on the diuretic.

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References

  1. Helgeland A (1980) Treatment of mild hypertension. A five-years controlled drug trial. The Oslo Study. Am J Med 69: 725–732

    Google Scholar 

  2. Multiple risk factor intervention trial research group (1982) Multiple risk factor intervention trial. J Am Med Assoc 248: 1465–1477

    Google Scholar 

  3. Veterans administration cooperative study group on antihypertensive agents (1967) Effects of treatment on morbidity in hypertension. J Am Med Assoc 202: 1028–1034

    Google Scholar 

  4. Ames RP, Hill P (1982) Improvement of glucose tolerance and lowering of glycohemoglobin and serum lipid concentrations after discontinuation of antihypertensive drug therapy. Circulation 65: 899–904

    Google Scholar 

  5. Ames RP (1983) Negative effects of diuretic drug on metabolic risk factors for coronary heart disease. Possibly alternative drug therapies. Am J Cardiol 51: 632–638

    Google Scholar 

  6. Andersen OO, Persson I (1968) Carbohydrate metabolism during treatment with chlorthalidone and ethacrynic acid. Br Med J 2: 798–801

    Google Scholar 

  7. Editorial (1980) Antihypertensive drugs, plasma lipids, and coronary disease. Lancet 2: 19–20

  8. Editorial (1982) Calcium antagonists in hypertension. Lancet 2: 307–308

  9. Mikać-Devic H, Stancovic H, Boskovic K (1973) A method for determination of free fatty acids in serum. Clin Chim Acta 45: 55–59

    Google Scholar 

  10. Viikari J (1976) Precipitation of plasma lipoproteins by PEG-6000 and its evaluation with electrophoresis and ultracentrifugation. Scand J Clin Lab Invest 36: 265–268

    Google Scholar 

  11. Beaumont JJ, Carlson LA, Cooper GR, Fejfar Z, Fredrickson DS, Strasser T (1970) Classification of hyperlipidaemias and hyperlipoproteinaemias. Bull WHO 43: 891

    Google Scholar 

  12. Faber O, Binder C (1977) C-peptide response to glucagon: a test for residual function in diabetes mellitus. Diabetes 26: 605–610

    Google Scholar 

  13. Fossati P, Prencipe L, Berti G (1980) Use of 3,5-dichloro-2-hydroxybenzenesulfanic acid 4-aminophenazone chromogenic system in direct enzymic assay of uric acid in serum and urine. Clin Chem 26: 227–231

    Google Scholar 

  14. Scheffe H (1959) The analysis of variance. Wiley, New York

    Google Scholar 

  15. Gould BA, Mann S, Kieso H, Balasubramanian V, Raftery EB (1982) The role of a slow channel inhibitor, verapamil, in the management of hypertension. Clin Exp Pharmacol Physiol 6 [Suppl]: 113–121

    Google Scholar 

  16. Lewis GRJ (1982) The long-term management of hypertension with verapamil. Clin Exp Pharmacol Physiol 6 [Suppl]: 107–112

    Google Scholar 

  17. Midbø K, Hals O (1980) Verapamil in the treatment of hypertension. Curr Ther Res 27: 830–838

    Google Scholar 

  18. Hulthen UL, Bolli P, Bühler FR (1984) Calcium influx blockers in the treatment of hypertension. Acta Med Scand 681 [Suppl]: 101–108

    Google Scholar 

  19. Bühler FR, Hulthen UL, Kiowski W, Müller FB, Bolli P (1982) The place of the calcium antagonist verapamil in antihypertensive therapy. J Cardiovasc Pharmacol 4 [Suppl 3]: 350–357

    Google Scholar 

  20. Amery A, Birkenhager W, Bulpitt C, Clement D, Deruyttere M, Deschaepdryver A, Dollery C, Fagard R, Forette F, Forte J, Hamdy R, Leonetti G, Lund-Johansen P, Macfarlane JPR, Mutsers A, Omalley K, Tuomilehto J (1982) Influence of antihypertensive therapy on serum cholesterol in elderly hypertensive patients. Acta Cardiol 37: 235–244

    Google Scholar 

  21. Bengtsson C, Lennartsson J, Lindquist O, Lindstedt G, Lundberg PA, Noppa H, Sigurdsson JA, Tibblin E (1982) On metabolic effects of diuretics and β-blockers. Acta Med Scand 212: 57–64

    Google Scholar 

  22. Veterans Administration Co-operative Study Group on Antihypertensive Agents (1982) Comparison of propranolol and hydrochlorothiazide for the initial treatment of hypertension. II. Results of long-term therapy. J Am Med Assoc 248: 2004–2011

    Google Scholar 

  23. Wallace RB, Hunninghake DB, Reiland S, Barrettconnor E, Mackenthun A, Hoover J, Wahl P (1980) Alterations of plasma high-density lipoprotein cholesterol levels associated with consumption of selected medications. Circulation 62: 77–82

    Google Scholar 

  24. Glück Z, Weidmann P, Mordasini R, Bachmann C, Riesen W, Peheim E, Keusch G, Meier A (1980) Increased serum low-density lipoprotein cholesterol in men treated short-term with the diuretic chlortalidone. Metabolism 29: 240–245

    Google Scholar 

  25. Glück Z, Baumgartner G, Weidmann P, Peheim E, Bachmann C, Mordasini R, Flammer J, Keusch G (1978) Increased ratio between serum beta- and alpha-lipoproteins during diuretic therapy: an adverse effect. Clin Sci Mol Med 55: 3255–3285

    Google Scholar 

  26. Grimm RH, Leon AS, Hunninghake DB, Lenz K, Hannen P, Blackburn H (1981) Effects of thiazide diuretics on plasma lipids and lipoproteins in mildly hypertensive patients. Ann Intern Med 94: 7–11

    Google Scholar 

  27. Johnson BF (1982) The emerging problem of plasma lipid changes during antihypertensive therapy. J Cardiovasc Pharmacol 4 [Suppl 2]: S 213–221

    Google Scholar 

  28. Ames RP, Hill P (1982) Anithypertensive therapy and the risk of coronary heart disease. J Cardiovasc Pharmacol 4 [Suppl 2]: S 206–212

    Google Scholar 

  29. DeMarinis L, Barbarino A (1980) Calcium antagonists and hormone release I. Effects of verapamil on insulin release in normal subjects and patients with islet-cell tumor. Metabolism 24: 599–604

    Google Scholar 

  30. Charles S, Ketelslegers J-M, Buysschaert M, Lambert AE (1981) Hyperglycaemic effect of nifedipine. Br Med J 283: 19–20

    Google Scholar 

  31. Katz AM, Reuter H (1979) Cellular calcium and cardiac cell death. Am J Cardiol 44: 188–190

    Google Scholar 

  32. Nayler WG (1981) The heart cell: some metabolic aspects or cardiac arrhythmias. Acta Med Scand 647 [Suppl]: 17–31

    Google Scholar 

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Lehtonen, A., Gordin, A. Metabolic parameters after changing from hydrochlorothiazide to verapamil treatment in hypertension. Eur J Clin Pharmacol 27, 153–157 (1984). https://doi.org/10.1007/BF00544038

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