We investigated whether the anionic component of an orally administered sodium salt can influence the salt's capacity to increase blood pressure. In five men with essential hypertension in whom blood pressure was normal with restriction of dietary sodium chloride to 10 mmol per day (0.23 g of sodium per day), oral administration of sodium chloride for seven days, 240 mmol per day (5.52 g of sodium per day), induced significant increases in systolic and diastolic blood pressures, of 16 +/- 2 and 8 +/- 2 mm Hg (mean +/- SEM), respectively (P less than 0.05). An equimolar amount of sodium given as sodium citrate induced no change in blood pressure. Replacing supplemental sodium chloride with an equimolar amount of sodium as sodium citrate abolished the increase in blood pressure induced by sodium chloride. Both salts induced substantial and comparable sodium retention, weight gain, and suppression of plasma renin activity and plasma aldosterone, but supplemental sodium chloride increased plasma volume and urinary excretion of calcium, whereas sodium citrate did not. These preliminary findings demonstrate that the anionic component of an orally administered sodium salt can influence the ability of that salt to increase blood pressure, possibly by determining whether the salt induces an increase in plasma volume. Our observations in a small group of men with salt-sensitive hypertension will require confirmation in larger numbers of patients of both sexes.
Source Information
Department of Laboratory Medicine, University of California at San Francisco 94143-0126.
This article has been cited by other articles:
McCarron, D. A.
(2008). Dietary sodium and cardiovascular and renal disease risk factors: dark horse or phantom entry?. Nephrol Dial Transplant
23: 2133-2137
[Full Text]
Schmidlin, O., Forman, A., Sebastian, A., Morris, R. C. Jr
(2007). Sodium-Selective Salt Sensitivity: Its Occurrence in Blacks. Hypertension
50: 1085-1092
[Abstract][Full Text]
Kim, Y. H., Pech, V., Spencer, K. B., Beierwaltes, W. H., Everett, L. A., Green, E. D., Shin, W., Verlander, J. W., Sutliff, R. L., Wall, S. M.
(2007). Reduced ENaC protein abundance contributes to the lower blood pressure observed in pendrin-null mice. Am. J. Physiol. Renal Physiol.
293: F1314-F1324
[Abstract][Full Text]
Taylor, E. N., Forman, J. P., Farwell, W. R.
(2007). Serum Anion Gap and Blood Pressure in the National Health and Nutrition Examination Survey. Hypertension
50: 320-324
[Abstract][Full Text]
Schafflhuber, M., Volpi, N., Dahlmann, A., Hilgers, K. F., Maccari, F., Dietsch, P., Wagner, H., Luft, F. C., Eckardt, K.-U., Titze, J.
(2007). Mobilization of osmotically inactive Na+ by growth and by dietary salt restriction in rats. Am. J. Physiol. Renal Physiol.
292: F1490-F1500
[Abstract][Full Text]
Schmidlin, O., Forman Anthony Sebastian, A., Morris, R. C. Jr
(2007). What Initiates the Pressor Effect of Salt in Salt-Sensitive Humans?: Observations in Normotensive Blacks. Hypertension
49: 1032-1039
[Abstract][Full Text]
Verlander, J. W., Kim, Y. H., Shin, W., Pham, T. D., Hassell, K. A., Beierwaltes, W. H., Green, E. D., Everett, L., Matthews, S. W., Wall, S. M.
(2006). Dietary Cl- restriction upregulates pendrin expression within the apical plasma membrane of type B intercalated cells. Am. J. Physiol. Renal Physiol.
291: F833-F839
[Abstract][Full Text]
Vallet, M., Picard, N., Loffing-Cueni, D., Fysekidis, M., Bloch-Faure, M., Deschenes, G., Breton, S., Meneton, P., Loffing, J., Aronson, P. S., Chambrey, R., Eladari, D.
(2006). Pendrin Regulation in Mouse Kidney Primarily Is Chloride-Dependent. J. Am. Soc. Nephrol.
17: 2153-2163
[Abstract][Full Text]
Schmidlin, O., Tanaka, M., Bollen, A. W., Yi, S.-L., Morris, R. C. Jr
(2005). Chloride-Dominant Salt Sensitivity in the Stroke-Prone Spontaneously Hypertensive Rat. Hypertension
45: 867-873
[Abstract][Full Text]
Aviv, A., Hollenberg, N. K., Weder, A.
(2004). Urinary Potassium Excretion and Sodium Sensitivity in Blacks. Hypertension
43: 707-713
[Abstract][Full Text]
McCarron, D. A
(2000). The dietary guideline for sodium: should we shake it up? Yes!. Am. J. Clin. Nutr.
71: 1013-1019
[Abstract][Full Text]
Safar, M.E, Thuilliez, C., Richard, V, Benetos, A
(2000). Pressure-independent contribution of sodium to large artery structure and function in hypertension. Cardiovasc Res
46: 269-276
[Abstract][Full Text]
Schmidlin, O., Forman, A., Tanaka, M., Sebastian, A., Morris, R. C. Jr
(1999). NaCl-Induced Renal Vasoconstriction in Salt-Sensitive African Americans : Antipressor and Hemodynamic Effects of Potassium Bicarbonate. Hypertension
33: 633-639
[Abstract][Full Text]
Graudal, N. A., Galloe, A. M., Garred, P.
(1998). Effects of Sodium Restriction on Blood Pressure, Renin, Aldosterone, Catecholamines, Cholesterols, and Triglyceride: A Meta-analysis. JAMA
279: 1383-1391
[Abstract][Full Text]
Tanaka, M., Schmidlin, O., Yi, S.-L., Bollen, A. W., Morris, R. C. Jr.
(1997). Genetically determined chloride-sensitive hypertension and stroke. Proc. Natl. Acad. Sci. USA
94: 14748-14752
[Abstract][Full Text]
Weinberger, M. H.
(1996). Salt Sensitivity of Blood Pressure in Humans. Hypertension
27: 481-490
[Abstract][Full Text]
Weir, M. R., Dengel, D. R., Behrens, M. T., Goldberg, A. P.
(1995). Salt-Induced Increases in Systolic Blood Pressure Affect Renal Hemodynamics and Proteinuria. Hypertension
25: 1339-1344
[Abstract][Full Text]
(1987). SALT-SENSITIVE HYPERTENSION: IS CHLORIDE A CULPRIT?. JWatch General
1987: 2-2
[Full Text]
Previous
