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(Hypertension. 1999;34:882-888.)
© 1999 American Heart Association, Inc.

Scientific Contributions

Enhanced Vascular Reactivity and Ca²⁺ Entry With Low-Salt Diet

Effect of Obesity

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

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

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 Ca²⁺-dependent mechanisms of vasoconstriction are unclear. The purpose of this study was to investigate the effect of low salt diet on vascular reactivity and Ca²⁺ mobilization mechanisms and the modulation of these effects with obesity. Active stress and ⁴⁵Ca²⁺ 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 Ca²⁺–dependent increases in active stress and ⁴⁵Ca²⁺ influx. In lean rabbits, the Phe- and KCl-induced stress and Ca²⁺ influx were significantly greater with the low-salt versus the normal-salt diet. The Phe-induced Ca²⁺ 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 Ca²⁺ influx were significantly less than that in lean rabbits but the Ca²⁺ 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 Ca²⁺ influx but also with significant enhancement in the Ca²⁺ influx-stress relationship. In Ca²⁺-free (2 mmol/L EGTA) Krebs solution, stimulation of intracellular Ca²⁺ 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 Ca²⁺ entry and vascular reactivity. Low-salt diet is associated with an increase in Ca²⁺ entry and vascular reactivity in both obese and lean rabbits. The enhancement of the Ca²⁺ influx-stress relationship with low-salt diet, particularly in the obese rabbits, suggests activation of other contractile mechanisms in addition to Ca²⁺ entry.

Key Words: diet • resistance, vascular • calcium • muscle, smooth, vascular • contraction

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