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(Hypertension. 2002;39:368.)
© 2002 American Heart Association, Inc.

Scientific Contributions

Low-Salt Diet Enhances Vascular Reactivity and Ca²⁺ Entry in Pregnant Rats With Normal and Reduced Uterine Perfusion Pressure

Jena B. Giardina; Kathy L. Cockrell; Joey P. Granger; Raouf A. Khalil

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

Correspondence to Raouf A. Khalil, MD, PhD, Department of Physiology & Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216. E-mail rkhalil{at}physiology.umsmed.edu

Salt moderation is often recommended to prevent excessive increases in blood pressure during pregnancy, particularly in women who are prone to pregnancy-induced hypertension; however, the vascular effects of low dietary salt intake during pregnancy are unclear. We investigated whether a low-salt diet during pregnancy alters the mechanisms of vascular smooth muscle contraction. Active stress and ⁴⁵Ca²⁺ influx were measured in endothelium-denuded aortic strips of virgin and normal pregnant Sprague-Dawley rats and a hypertensive pregnant rat model produced by reduction in uterine perfusion pressure (RUPP), fed either a normal-sodium (NS, 1% NaCl) or low-sodium diet (LS, 0.2% NaCl) for 7 days. The mean arterial pressure was as follows: virgin/NS 108±8, virgin/LS 117±7, pregnant/NS 102±3, pregnant/LS 117±4, RUPP/NS 119±3, and RUPP/LS 133±6 mm Hg. Phenylephrine (Phe) caused concentration-dependent increases in active stress and ⁴⁵Ca²⁺ influx that were greater in RUPP rats than in normal pregnant or virgin rats and were enhanced in pregnant/LS and RUPP/LS compared with pregnant/NS and RUPP/NS, respectively. High KCl (16 to 96 mmol/L), which stimulates Ca²⁺ entry from the extracellular space, also caused increases in active stress that were greater in RUPP than in normal pregnant, in pregnant/LS than in pregnant/NS, and in RUPP/LS than in RUPP/NS rats. The Phe-induced ⁴⁵Ca²⁺ influx–active stress relation was greater in RUPP/NS than in pregnant/NS and was enhanced in pregnant/LS and RUPP/LS compared with pregnant/NS and RUPP/NS, respectively. In Ca²⁺-free (2 mmol/L ethylene glycol bis(ß-aminoethylether)-N,N,N',N'-tetra-acetic acid) Krebs, stimulation of intracellular Ca²⁺ release by Phe (10^-5 mol/L) or caffeine (25 mmol/L) caused a transient contraction that was not significantly different in all groups of rats. Thus, a low-salt diet in pregnant and RUPP rats is associated with increases in vascular reactivity that involves Ca²⁺ entry from the extracellular space but not Ca²⁺ release from the intracellular stores. The enhancement of the Phe-induced Ca²⁺ influx–active stress relation in pregnant and RUPP rats on a low-salt diet suggests activation of other vascular contraction mechanisms in addition to Ca²⁺ entry. Although it is difficult to extrapolate the experimental data in rats to clinical data in women, the increased vascular reactivity and Ca²⁺ entry and the possible enhancement of additional vascular contraction mechanisms with a low-salt diet suggest that reduction of dietary salt intake should be carefully monitored during pregnancy and pregnancy-induced hypertension.

Key Words: arterial pressure • muscle, smooth, vascular • calcium

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