Enhanced Vascular Reactivity and Ca 2+ Entry With Low-Salt Diet

Author:

Khalil Raouf A.1,Crews Janice K.1,Carroll Joan F.1,Hall John E.1

Affiliation:

1. From the Department of Physiology and Biophysics and the Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Miss.

Abstract

Abstract —Salt moderation is often recommended as a nonpharmacological therapy for hypertension, particularly in overweight individuals; however, the effects of low dietary salt on the Ca 2+ -dependent mechanisms of vasoconstriction are unclear. The purpose of this study was to investigate the effect of low salt diet on vascular reactivity and Ca 2+ mobilization mechanisms and the modulation of these effects with obesity. Active stress and 45 Ca 2+ influx were measured in deendothelialized aortic strips isolated from lean (3.74 kg) and obese (5.51 kg) female rabbits on a normal (0.75%) or low (0.23%) salt (sodium chloride) diet for 18 weeks. Both phenylephrine (Phe, 10 −5 mol/L) and membrane depolarization by 96 mmol/L KCl caused extracellular Ca 2+ –dependent increases in active stress and 45 Ca 2+ influx. In lean rabbits, the Phe- and KCl-induced stress and Ca 2+ influx were significantly greater with the low-salt versus the normal-salt diet. The Phe-induced Ca 2+ influx–stress relationship was significantly greater than that induced by KCl with low-salt diet. In obese rabbits on a normal-salt diet, the Phe- and KCl-induced stress and Ca 2+ influx were significantly less than that in lean rabbits but the Ca 2+ influx-stress relationship was not significantly altered. Feeding the obese rabbits a low-salt diet was associated not only with significant increases in Phe- and KCl-induced active stress and Ca 2+ influx but also with significant enhancement in the Ca 2+ influx-stress relationship. In Ca 2+ -free (2 mmol/L EGTA) Krebs solution, stimulation of intracellular Ca 2+ release by Phe or caffeine (25 mmol/L) caused a transient contraction that was not significantly different in all groups of rabbits. Thus, with normal salt intake, obesity is associated with a reduction in Ca 2+ entry and vascular reactivity. Low-salt diet is associated with an increase in Ca 2+ entry and vascular reactivity in both obese and lean rabbits. The enhancement of the Ca 2+ influx-stress relationship with low-salt diet, particularly in the obese rabbits, suggests activation of other contractile mechanisms in addition to Ca 2+ entry.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Internal Medicine

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