PARENT SESSION
Nutrition and Reproduction

EFFECTS OF LOW AND HIGH SODIUM DIETS ON SIZE AND REACTIVITY OF THE UTERINE ARCUATE ARTERIES OF NON-PREGNANT AND PREGNANT RATS.

St-Louis, Jean¹, Sicotte, Benoit¹, Beauséjour, Annie¹, Auger, Karine¹, Brochu, Michèle¹, ¹

ABSTRACT- We have shown that ingestion of low sodium diet by pregnant rats increases the activation of the renin-angiotensin-aldosterone system (RAAS) and reduces the increase in blood volume. It is also associated to birth of pups with intrauterine growth restriction. We investigated the effects of low and high sodium diets on size and reactivity to angiotensin II (AngII) of the uterine vasculature. Non-pregnant and pregnant rats received normal diet, low sodium (0.03%) or normal diet plus saline (NaCl 0.9%) as beverage for 7 days, e.g., for the last of the 3 weeks of gestation. Rats were sacrificed after 7 days treatment (22nd day gestation) to pick up the uterine vascular bed and plasma. Uterine arcuate arteries (>100 m, diam.) were dissected and set up in a wire myograph systems under a passive tension equivalent to 50 mmHg transmural pressure (length-tension curve). Concentration-response curves to AngII were obtained in the absence and presence of losartan (100 nM). Under normal diet, diameter of the arcuate artery doubled during pregnancy, but this remodeling was reduced under both low and high sodium. Compared to normal diet, the low sodium markedly increased responsiveness to AngII on the arcuate arteries of non-pregnant rats. Pregnancy also resulted in increased responses to AngII. However, with low sodium diet, the arteries of pregnant rats showed reduced sensitivity and responsiveness to the peptide. In this condition, the inhibitory effect of losartan on AngII responses was also reduced. High sodium diet did not affect reactivity of the uterine arcuate arteries of both non-pregnant and pregnant rats. The present data show that low sodium diet in non-pregnant rats induced an important increase in reactivity of the uterine arteries to AngII and suggest that the over-increased of the RAAS, induced by the low sodium diet in pregnant rats, markedly reduced reactivity to AngII. RAAS suppression by high sodium diet did not show any impact on reactivity to AngII.

KEY WORDS: Uterine Artery, sodium diet, pregnancy, angiotensin