Giardina Jena B, Cockrell Kathy L, Granger Joey P, Khalil Raouf A
Department of Physiology and Biophysics and Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, MS 39216, USA.
Hypertension. 2002 Feb;39(2 Pt 2):368-74. doi: 10.1161/hy02t2.102806.
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 (45)Ca(2+) 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 (45)Ca(2+) 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 Ca(2+) 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 (45)Ca(2+) 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 Ca(2+)-free (2 mmol/L ethylene glycol bis(beta-aminoethylether)-N,N,N',N'-tetra-acetic acid) Krebs, stimulation of intracellular Ca(2+) 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 Ca(2+) entry from the extracellular space but not Ca(2+) release from the intracellular stores. The enhancement of the Phe-induced Ca(2+) influx--active stress relation in pregnant and RUPP rats on a low-salt diet suggests activation of other vascular contraction mechanisms in addition to Ca(2+) entry. Although it is difficult to extrapolate the experimental data in rats to clinical data in women, the increased vascular reactivity and Ca(2+) 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.
通常建议适度摄入盐分，以防止孕期血压过度升高，尤其是对于易患妊娠高血压的女性；然而，孕期低钠饮食对血管的影响尚不清楚。我们研究了孕期低钠饮食是否会改变血管平滑肌收缩的机制。对未孕和正常怀孕的斯普拉格-道利大鼠以及通过降低子宫灌注压（RUPP）产生的高血压怀孕大鼠模型的去内皮主动脉条进行活性张力和（45）Ca（2+）内流测量，这些大鼠分别喂食正常钠（NS，1% NaCl）或低钠饮食（LS，0.2% NaCl）7天。平均动脉压如下：未孕/NS 108±8，未孕/LS 117±7，怀孕/NS 102±3，怀孕/LS 117±4，RUPP/NS 119±3，以及RUPP/LS 133±6 mmHg。去氧肾上腺素（Phe）引起活性张力和（45）Ca（2+）内流呈浓度依赖性增加，RUPP大鼠中的增加幅度大于正常怀孕或未孕大鼠，并且与怀孕/NS和RUPP/NS相比，怀孕/LS和RUPP/LS中的增加幅度更大。高钾（16至96 mmol/L）刺激细胞外空间的Ca（2+）内流，也导致活性张力增加，RUPP大鼠中的增加幅度大于正常怀孕大鼠，怀孕/LS大于怀孕/NS，RUPP/LS大于RUPP/NS大鼠。Phe诱导的（45）Ca（2+）内流-活性张力关系在RUPP/NS中大于怀孕/NS，并且与怀孕/NS和RUPP/NS相比，怀孕/LS和RUPP/LS中的关系增强。在无Ca（2+）（2 mmol/L乙二醇双（β-氨基乙基醚）-N，N，N'，N'-四乙酸）的 Krebs液中，Phe（10（-5）mol/L）或咖啡因（25 mmol/L）刺激细胞内Ca（2+）释放引起短暂收缩，所有大鼠组之间无显著差异。因此，怀孕和RUPP大鼠的低钠饮食与血管反应性增加有关，这涉及细胞外空间的Ca（2+）内流，但不涉及细胞内储存的Ca（2+）释放。低钠饮食的怀孕和RUPP大鼠中Phe诱导的Ca（2+）内流-活性张力关系增强表明，除了Ca（2+）内流外，其他血管收缩机制也被激活。尽管很难将大鼠的实验数据外推至女性的临床数据，但低钠饮食导致的血管反应性增加、Ca（2+）内流增加以及其他血管收缩机制可能增强，这表明在孕期和妊娠高血压期间应仔细监测饮食盐摄入量的减少。
