Perinatal programming of hypertension : the effect of high and low maternal dietary salt intake on the blood pressure : of the offspring in Sprague Dawley rats

Abstract

Adverse conditions in utero may lead to hypertension in later life. One model of perinatal programming includes the effects of high and low maternal dietary salt intake on the offspring‟s systolic blood pressure in adult life. The main aims of the study are to investigate the effects of different maternal dietary salt intake [low salt diet (LSD) (0.145%NaCl), normal salt diet (NSD) (1.0%NaCl) and high salt diet (HSD) (3.0%NaCl) group] during pregnancy and lactation on the 1) offspring‟s baseline systolic blood pressure at 4,8,12 weeks of life and upon 1-month of high dietary salt challenge. 2) baseline plasma renin activity at 12 weeks of life and upon 1-month of high dietary salt challenge. Female rats were fed either LSD (n=10), NSD (n=10) or HSD (n=10) during pregnancy and lactation. At 4 weeks of life all offspring were fed with NSD until 12 weeks of life and then challenged with HSD for 4 weeks. Offspring‟s systolic blood pressure was measured at 4,8,12 and 16 weeks of life. Plasma renin activity was measured at 12 and 16 weeks of life. At 4,8,12 and weeks of life, HSD dams offspring‟s have significantly higher systolic blood pressure than NSD dams offspring‟s respectively (4 weeks: 119.44mmHg ±1.8 vs 103.65mmHg ±0.92; 8 weeks: 131.06±1.49mmHg vs 120.26mmHg±1.09; 12 weeks: 137.29mmHg±1.41 vs 128.77mmHg±1.77 and 16 weeks: 143.04±3.09mmHg vs 131.45±1.37mmHg). At 8,12 and 16 weeks of life, LSD dams offspring‟s have significantly higher systolic blood pressure than NSD dams offspring‟s respectively (8 weeks; 130.13±1.45mmHg vs 120.26mmHg±1.09; 12 weeks: 134.71±1.13mmHg vs 128.77±1.77 mmHg and 16 weeks: 141.87±1.04mmHg vs 131.45±1.37mmHg). Plasma renin activity was similar among the groups at 12 and 16 weeks of life. The offspring of both HSD and LSD dams have greater propensity to develop higher systolic blood pressure. This suggests the importance of maternal dietary salt optimization. Plasma renin activity is not the mechanisms of the perinatal programming of hypertension in this study.