High-sodium intake prevents pregnancy-induced decrease of blood pressure in the rat

American Journal of Physiology - Heart and Circulatory Physiology - Tập 285 Số 1 - Trang H375-H383 - 2003
Annie Beauséjour1, Karine Auger1, Jean St‐Louis1, Martin Brochu1
1Research Centre, Hôpital Sainte-Justine, and Department of Obstetrics and Gynecology, Université de Montreal, Montreal, Quebec, Canada H3T 1C5

Tóm tắt

Despite an increase of circulatory volume and of renin-angiotensin-aldosterone system (RAAS) activity, pregnancy is paradoxically accompanied by a decrease in blood pressure. We have reported that the decrease in blood pressure was maintained in pregnant rats despite overactivation of RAAS following reduction in sodium intake. The purpose of this study was to evaluate the impact of the opposite condition, e.g., decreased activation of RAAS during pregnancy in the rat. To do so, 0.9% or 1.8% NaCl in drinking water was given to nonpregnant and pregnant Sprague-Dawley rats for 7 days (last week of gestation). Increased sodium intakes (between 10- and 20-fold) produced reduction of plasma renin activity and aldosterone in both nonpregnant and pregnant rats. Systolic blood pressure was not affected in nonpregnant rats. However, in pregnant rats, 0.9% sodium supplement prevented the decreased blood pressure. Moreover, an increase of systolic blood pressure was obtained in pregnant rats receiving 1.8% NaCl. The 0.9% sodium supplement did not affect plasma and fetal parameters. However, 1.8% NaCl supplement has larger effects during gestation as shown by increased plasma sodium concentration, hematocrit level, negative water balance, proteinuria, and intrauterine growth restriction. With both sodium supplements, decreased AT1mRNA levels in the kidney and in the placenta were observed. Our results showed that a high-sodium intake prevents the pregnancy-induced decrease of blood pressure in rats. Nonpregnant rats were able to maintain homeostasis but not the pregnant ones in response to sodium load. Furthermore, pregnant rats on a high-sodium intake (1.8% NaCl) showed some physiological responses that resemble manifestations observed in preeclampsia.

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Tài liệu tham khảo

10.1161/01.HYP.37.4.1191

August P.Hypertensive disorders in pregnancy. In:Medical Complications During Pregnancy, edited by Burrow GN and Duffy TP. Philadelphia, PA: Saunders, 1999, p. 53-77.

10.1161/01.HYP.38.3.730

10.1016/S0272-6386(87)80125-7

10.1016/S0304-3940(97)13375-4

Bell PDand Peti-Peterdi J.Angiotensin II stimulates macula densa basolaterale sodium/hydrogen exchange via type angiotensin receptors.J Am Soc Nephrol10: S225-S229, 1999.

10.1016/0031-9384(86)90247-7

Bohlender J, Ganten D, and Luft FC.Rats transgenic for human renin and human angiotensinogen as a model for gestational hypertension.J Am Soc Nephrol11: 2056-2061, 2000.

10.1152/ajpendo.1997.272.1.E18

Chomczynski Pand Sacci N.Single-step method of RNA isolation by acid guanidium thiocyanate-phenol-chloroform extraction.Anal Biochem162: 156-159, 1987.

10.1016/0002-9378(88)90090-7

10.1530/eje.0.1420524

Duley Land Henderson-Smart D.Reduced salt intake compared with normal dietary salt, or high intake, in pregnancy.Cochrane Database Syst Rev2: CD001687, 2000.

10.1097/00006254-199412000-00007

10.1172/JCI107462

10.1677/joe.0.1130435

Gutkowska J, Boucher R, and Genest J.Dosage radioimmunologique de l'activite renine plasmatique.Union Med Can106: 446-450, 1977.

10.1152/ajpregu.2001.280.1.R174

10.1046/j.1440-1681.1999.03158.x

10.1161/01.HYP.31.1.315

Knock GA, Sullivan MH, McCarthy A, Elder MG, Polak JM, and Wharton J.Related articles angiotensin II (AT1) vascular binding sites in human placentae from normal-term, preeclamptic and growth retarded pregnancies.J Pharmacol Exp Ther271: 1007-1015, 1994.

10.1016/S0031-9384(98)00144-9

10.1172/JCI119881

Lockwood CJand Paidas MJ.Preeclampsia and hypertensive disorders. In:Cherry and Merkatz's Complications of Pregnancy(5th ed.), edited by Cohen WR. Philadelphia, PA: Lippincott, Williams and Wilkins, 2000, p. 207-214.

10.1111/j.1440-1681.1985.tb02654.x

10.1016/0002-9378(83)90967-5

10.1016/S0002-9378(13)90488-9

Moutquin JM, Bilodeau R, Raynault P, Amyot G, Blair JF, Labelle L, Rainville C, and Gagnon L.Étude prosprective de la tension artérielle au cours de la grossesse. Prédiction des complications hypertensives.J Gynecol Obstet Biol Reprod (Paris)11: 833-837, 1982.

10.1093/jn/101.2.169

10.1016/S0146-0005(99)80055-X

10.1016/S0002-9378(99)70262-0

10.3109/10641959809072239

10.1161/01.HYP.29.4.923

10.1152/ajpheart.01183.2000

10.1016/0028-2243(91)90097-5

10.1016/0024-3205(85)90251-6

10.1097/00003081-199409000-00009

Uzan S, Beaufils M, and Uzan M.HTA et grossesse. In:Obstétrique, edited by Papiernik E, Carbol D, and Pons JC. Paris: Flammarion, 1998, p. 793-824, 1998.

10.1152/jappl.1972.32.5.712

10.1038/ng0593-59

10.1097/00004872-199103000-00008

Wilson M, Morganti AA, Zervoudakis I, Letcher RL, Romney BM, Von Oeyon P, Papera S, Sealy JE, and Laragh JH.Blood pressure, the renin-aldosterone system and sex steroids throughout normal pregnancy.Am J Med86: 97-104, 1980.

10.1007/s004240050349

10.1677/joe.0.1500231

10.1016/0002-9378(93)90299-X

Youmbissi TJ, Tedong F, Tapser S, and Nash BT.The level of plasma renin and plasma aldosterone activity in normotensive women and in pregnancy-induced arterial hypertension in a group of women from Cameroon.J Gynecol Obstet Biol Reprod (Paris)20: 802-804, 1991.

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American Journal of Physiology - Heart and Circulatory Physiology

Tập 285 Số 1

H375-H383

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