title: High-sodium intake prevents pregnancy-induced decrease of blood pressure in the rat.
abstract: 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 AT1 mRNA 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.
authors.affiliation: Hôpital Sainte-Justine, Department of Obstetrics and Gynecology, Université de Montreal, Montreal, Quebec, Canada H3T 1C5.
authors.forename: Annie
authors.initials: A
authors.lastname: Beauséjour
authors.forename: Karine
authors.initials: K
authors.lastname: Auger
authors.forename: Jean
authors.initials: J
authors.lastname: St-Louis
authors.forename: Michéle
authors.initials: M
authors.lastname: Brochu
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D003404:Creatinine / Q000097:blood; D004435:Eating / Q000502:physiology; D004573:Electrolytes / Q000097:blood; D005260:Female; D020567:Fetal Weight / Q000187:drug effects / Q000502:physiology; D006400:Hematocrit; D006706:Homeostasis / Q000502:physiology; D006728:Hormones / Q000097:blood; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D023282:Nuclease Protection Assays; D009929:Organ Size / Q000187:drug effects / Q000502:physiology; D010920:Placenta / Q000187:drug effects / Q000502:physiology; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000502:physiology*; D015347:RNA Probes; D012333:RNA, Messenger / Q000096:biosynthesis / Q000302:isolation & purification; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin / Q000096:biosynthesis; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D012964:Sodium / Q000097:blood; D012982:Sodium, Dietary / Q000494:pharmacology*; D014563:Urodynamics / Q000187:drug effects
chemical_list: D004573:Electrolytes; D006728:Hormones; D015347:RNA Probes; D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin; D012982:Sodium, Dietary; D012964:Sodium; D003404:Creatinine