Abstract
Nifedipine is now widely used for the treatment of both angina and hypertension [1]. Its blood pressure lowering effect has been shown to be due to its inhibition of calcium induced contraction of arteriolar smooth muscle, which leads to peripheral vasodilatation [2]. This effect on arteriolar smooth muscle has been shown to be greater the higher the blood pressure [3]. An early intravenous study with nifedipine showed that it also caused a natriuresis and diuresis [4]. Later studies confirmed that acutely nifedipine causes a loss of sodium, which is independent of haemodynamic changes [5–7], and one study detected a greater increase in sodium excretion in patients with hypertension than in normotensive subjects [8]. It seems to have been generally assumed, however, that this acute effect of nifedipine on sodium excretion does not result in any long-term reduction in sodium balance.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
MacGregor GA (1986) Hypertension. In: Krebs R (ed) Treatment of cardiovascular diseases by Adalat. Schattauer, New York; pp 231–258
Fleckenstein A (1983) History of calcium antagonists. Clin Res 52 [Suppl 1]:3–16
Robinson BF (1984) Altered calcium handling as a cause of primary hypertension. J Hypertens 2:453–460
Yokoyama S, Kaburagi T (1983) Clinical effects of intravenous nifedipine on renal function. J Cardiovasc Pharmacol 5:67–71
Ene HD, Williamson PJ, Roberts CJC, Waddel G (1985) The natriuresis following oral administration of the calcium antagonists, nifedipine and nitrendipine. Br J Clin Pharmacol 19:423–427
Zanchetti A, Stella A, Golin A (1985) Adrenergic sodium handling and the natriuretic action of calcium antagonists. J Cardiovasc Pharmacol 7 [Suppl 6]: 194–198
Luft FC, Aronoff GR, Sloan RS, Fineberg NS, Weinberger MH (1986) Calcium channel blockade with nitrendipine. Effects on sodium homeostasis, the renin-angiotensin system and the sympathetic nervous system in humans. Hypertension 7:438–442
Leonetti G, Cuspidi C, Sampieri L, Terzoli L, Zanchetti A (1982) Comparison of cardiovascular, renal and humoral effects of acute administration of two calcium channel blockers in normotensive and hypertensive subjects. J Cardiovasc Pharmacol 4 [Suppl 3]:319–324
George CF, Lewis PJ, Pétrie A (1975) Clinical experience with use of ultrasound sphygmomanometer. Br Heart J 37:804–807
Roulston JE, MacGregor GA (1978) Measurements of plasma renin activity by radioimmunoassay after prolonged cold storage. Clin Chim Acta 88:45–48
James VHT, Wilson GA (1976) Determination of aldosterone in biological fluids. In: Reid E (ed) Assay of drugs and other trace compounds in biological fluids. Methodological developments in biochemistry, vol 5. Elsevier, Amsterdam; pp 149–158
Sagnella GA, Markandu ND, Shore AC, MacGregor GA (1985) Effects of changes in dietary sodium intake and saline infusion on immunoreactive atrial natriuretic peptide in human plasma. Lancet ii: 1208–1211
Snedecor GW, Cochran WG (1980) Statistical methods. Iowa State University Press, Ames, Iowa
SPSS Inc (1983) SPSS user’s guide. McGraw-Hill, New York
Di Bona GF, Sawin LL (1984) Renal tubular site of action of felodipine. J Pharmacol Exp Ther 223:420–424
Bruun NE, Ibsen H, Skoot P, Toftdahl D, Giese J, Holstein-Rathlou NH (1988) Lithium clearance and renal tubular sodium handling during acute and long-term nifedipine treatment in essential hypertension. Clin Sei 75:609–613
Petersen V, Hvidt S, Thomsen K, Schou M (1974) Effect of prolonged thiazide treatment on renal lithium clearance. Br Med J iii: 143–145
Cappuccio FP, Markandu ND, MacGregor GA (1987) Calcium antagonists and sodium balance. Effect of changes in sodium intake and of the addition of a thiazide diuretic on the blood pressure lowering effect of nifedipine. J Cardiovasc Pharmacol 10 [Suppl 10]:57–60
MacGregor GA, Cappuccio FP, Markandu ND (1987) Sodium intake, high blood pressure and calcium channel blockers. Am J Med 82 [Suppl 3B]: 16–22
Cappuccio FP, Markandu ND, Tucker F, SagneUa GA, MacGregor GA (1986) Does a diuretic cause a further fall in blood pressure in hypertensive patients already on nifedipine? J Clin Hypertens 4:346–353
Cappuccio FP, Markandu ND, Tucker F, Shore AC, MacGregor GA (1987) A double-blind study of the blood pressure lowering effect of a thiazide diuretic in hypertensive patients already on nifedipine and a betablocker. J Hypertens 5:733–738
Salvetti A, Magagna A, Innocenti P et al. (1989) Chlorthalidone does not increase the hypotensive effect of nifedipine in essential hypertensives: a crossover multicentre study. J Hypertens 7 [Suppl 6]:250–251
Williams SA, Rayman G, Tooke JE (1986) Oedema caused by vasodilator therapy: evidence for impairment of posturally-induced vasoconstriction (abstract). Int J Microcirc Clin Exp 5:393
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1991 Springer-Verlag Berlin Heidelberg
About this paper
Cite this paper
Pevahouse, J.B., Markandu, N.D., Cappuccio, F.P., Buckley, M.G., Sagnella, G.A., MacGregor, G.A. (1991). Long-Term Reduction in Sodium Balance: Possible Additional Mechanism Whereby Nifedipine Lowers Blood Pressure. In: Lichtlen, P.R., Reale, A. (eds) Adalat. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-85498-9_11
Download citation
DOI: https://doi.org/10.1007/978-3-642-85498-9_11
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-642-85500-9
Online ISBN: 978-3-642-85498-9
eBook Packages: Springer Book Archive