Skip to main content
NCBI home page
The BMJ logoLink to The BMJ
. 1990 Sep 22;301(6752):580–584. doi: 10.1136/bmj.301.6752.580

Long term reduction in sodium balance: possible additional mechanism whereby nifedipine lowers blood pressure.

J B Pevahouse 1, N D Markandu 1, F P Cappuccio 1, M G Buckley 1, G A Sagnella 1, G A MacGregor 1
PMCID: PMC1663742  PMID: 2146983

Abstract

OBJECTIVE--To assess the changes in sodium excretion and sodium balance after withdrawal of long term nifedipine. DESIGN--Single blind, placebo controlled study in patients receiving fixed sodium and potassium intakes. SETTING--Blood pressure unit of a teaching hospital in south London. PATIENTS--Eight patients with mild to moderate uncomplicated essential hypertension who had been taking nifedipine 20 mg twice daily for at least six weeks. INTERVENTIONS--Withdrawal of nifedipine and replacement with matching placebo for one week. MAIN OUTCOME MEASURES--Urinary sodium excretion and cumulative sodium balance, body weight, plasma atrial natriuretic peptide concentrations, plasma renin activity and aldosterone concentrations, and blood pressure. RESULTS--During nifedipine withdrawal there was a significant reduction in urinary sodium excretion (day 1: -62.7 mmol/24 h; 95% confidence interval -90.3 to -35.0) and each patient retained a mean of 146 (SEM 26) mmol sodium over the week of replacement with placebo. Body weight and plasma atrial natriuretic peptide concentrations increased during the placebo period and seemed to be associated with the amount of sodium retained. Systolic blood pressure rose from 157 (9) to 165 (9) mmHg (95% confidence interval of difference -7.1 to 22.1) when nifedipine was replaced with matching placebo, and the rise seemed to be related to the amount of sodium that was retained. CONCLUSIONS--Nifedipine causes a long term reduction in sodium balance in patients with essential hypertension. This long term effect may contribute to the mechanism whereby nifedipine lowers blood pressure.

Full text

PDF
580

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Bruun N. E., Ibsen H., Skøtt P., Toftdahl D., Giese J., Holstein-Rathlou N. H. Lithium clearance and renal tubular sodium handling during acute and long-term nifedipine treatment in essential hypertension. Clin Sci (Lond) 1988 Dec;75(6):609–613. doi: 10.1042/cs0750609. [DOI] [PubMed] [Google Scholar]
  2. Cappuccio F. P., Markandu N. D., Tucker F. A., Shore A. C., MacGregor G. A. A double-blind study of the blood pressure lowering effect of a thiazide diuretic in hypertensive patients already on nifedipine and a beta-blocker. J Hypertens. 1987 Dec;5(6):733–738. doi: 10.1097/00004872-198712000-00017. [DOI] [PubMed] [Google Scholar]
  3. Cappuccio F. P., Markandu N. D., Tucker F., Sagnella G. A., MacGregor G. A. Does a diuretic cause a further fall in blood pressure in hypertensive patients already on nifedipine? J Clin Hypertens. 1986 Dec;2(4):346–353. [PubMed] [Google Scholar]
  4. Dibona G. F., Sawin L. L. Renal tubular site of action of felodipine. J Pharmacol Exp Ther. 1984 Feb;228(2):420–424. [PubMed] [Google Scholar]
  5. Ene M. D., Williamson P. J., Roberts C. J., Waddell G. The natriuresis following oral administration of the calcium antagonists--nifedipine and nitrendipine. Br J Clin Pharmacol. 1985 Apr;19(4):423–427. doi: 10.1111/j.1365-2125.1985.tb02665.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Fleckenstein A. History of calcium antagonists. Circ Res. 1983 Feb;52(2 Pt 2):I3–16. [PubMed] [Google Scholar]
  7. George C. F., Lewis P. J., Petrie A. Clinical experience with use of ultrasound sphygmomanometer. Br Heart J. 1975 Aug;37(8):804–807. doi: 10.1136/hrt.37.8.804. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Luft F. C., Aronoff G. R., Sloan R. S., Fineberg N. S., Weinberger M. H. Calcium channel blockade with nitrendipine. Effects on sodium homeostasis, the renin-angiotensin system, and the sympathetic nervous system in humans. Hypertension. 1985 May-Jun;7(3 Pt 1):438–442. [PubMed] [Google Scholar]
  9. MacGregor G. A., Cappuccio F. P., Markandu N. D. Sodium intake, high blood pressure, and calcium channel blockers. Am J Med. 1987 Mar 30;82(3B):16–22. doi: 10.1016/0002-9343(87)90206-3. [DOI] [PubMed] [Google Scholar]
  10. Petersen V., Hvidt S., Thomsen K., Schou M. Effect of prolonged thiazide treatment on renal lithium clearance. Br Med J. 1974 Jul 20;3(5924):143–145. doi: 10.1136/bmj.3.5924.143. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Robinson B. F. Altered calcium handling as a cause of primary hypertension. J Hypertens. 1984 Oct;2(5):453–460. doi: 10.1097/00004872-198410000-00002. [DOI] [PubMed] [Google Scholar]
  12. Roulston J. E., MacGregor G. A. Measurement of plasma renin activity by radioimmunoassay after prolonged cold storage. Clin Chim Acta. 1978 Aug 15;88(1):45–48. doi: 10.1016/0009-8981(78)90147-x. [DOI] [PubMed] [Google Scholar]
  13. Sagnella G. A., Markandu N. D., Shore A. C., MacGregor G. A. Effects of changes in dietary sodium intake and saline infusion on immunoreactive atrial natriuretic peptide in human plasma. Lancet. 1985 Nov 30;2(8466):1208–1211. doi: 10.1016/s0140-6736(85)90741-x. [DOI] [PubMed] [Google Scholar]
  14. Yokoyama S., Kaburagi T. Clinical effects of intravenous nifedipine on renal function. J Cardiovasc Pharmacol. 1983 Jan-Feb;5(1):67–71. doi: 10.1097/00005344-198301000-00010. [DOI] [PubMed] [Google Scholar]

Articles from BMJ : British Medical Journal are provided here courtesy of BMJ Publishing Group

RESOURCES