This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Fujita, T. Articles by Ito, Y. Search for Related Content PubMed PubMed Citation Articles by Fujita, T. Articles by Ito, Y.

Hypertension, Vol 21, 772-778, Copyright © 1993 by American Heart Association

ARTICLES

Salt loads attenuate potassium-induced vasodilation of forearm vasculature in humans

T Fujita and Y Ito
Fourth Department of Internal Medicine, University of Tokyo School of Medicine, Japan.

To evaluate the role of the sodium pump in resistance control in vivo, we studied vascular responses to potassium, which produces vasodilation by the activation of vascular Na+, K(+)-ATPase, in normotensive volunteers receiving a high salt diet compared with volume-depleted subjects receiving diuretic treatment. Forearm blood flow was measured by strain-gauge plethysmography during small increments in local concentrations of potassium with intrabrachial arterial infusions of KCl. Infusions of 0.12 and 0.24 mEq/min KCl increased forearm blood flow and decreased forearm vascular resistance in a dose-dependent fashion. But the simultaneous intrabrachial arterial infusion of 2 micrograms/min ouabain, a Na+,K(+)-ATPase inhibitor, could blunt the decremental response of vascular resistance to 0.12 mEq/min KCl. The decrements of vascular resistance with KCl infusions divided by the initial resistance were significantly less with ouabain compared with those without ouabain (43 +/- 4% versus 57 +/- 3%, p < 0.01). This suggests that potassium produces vasodilation by the activation of vascular Na+,K(+)-ATPase activity. Similarly, salt loading (180 mEq NaCl for 7 days) after treatment with diuretics could attenuate percent decrements of resistance with KCl infusions (39 +/- 3% versus 53 +/- 2%, p < 0.01), whereas vascular resistance responses to sodium nitroprusside, a nonspecific vasodilator, and to verapamil, a calcium antagonist, did not change with salt loading after volume depletion. Therefore, salt loading could attenuate forearm vascular response to potassium specifically, as did the administration of ouabain.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				P. Manunta, B. P. Hamilton, and J. M. Hamlyn Salt intake and depletion increase circulating levels of endogenous ouabain in normal men Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2006; 290(3): R553 - R559. [Abstract] [Full Text] [PDF]

				G. Dell'Omo, G. Penno, S. Del Prato, and R. Pedrinelli Chlorthalidone Improves Endothelial-Mediated Vascular Responses in Hypertension Complicated by Nondiabetic Metabolic Syndrome Journal of Cardiovascular Pharmacology and Therapeutics, October 1, 2005; 10(4): 265 - 272. [Abstract] [PDF]

				D. K. Wilson, D. A. Sica, and S. B. Miller Effects of Potassium on Blood Pressure in Salt-Sensitive and Salt-Resistant Black Adolescents Hypertension, August 1, 1999; 34(2): 181 - 186. [Abstract] [Full Text] [PDF]

				Y. Liu, N. J. Rusch, and J. H. Lombard Loss of Endothelium and Receptor-Mediated Dilation in Pial Arterioles of Rats Fed a Short-Term High Salt Diet Hypertension, February 1, 1999; 33(2): 686 - 688. [Abstract] [Full Text] [PDF]