Fetal programming on adult hypertension in pregnant rats under severe nutrition.

限制(R)组和对照组(C)的产仔数差异不显著(R组(9.3±0.7)，C组(10.6±0.7))。第1天，雄性和雌性R后代体重均显著低于C(R雄性：4.2±0.1g比C雄性；5.2±0.1g，R雌性；4.1±0.1g比C雌性；5.2±0.1g比C雌性)。R的雌性体重与C的雌性后代只有2周的差距。(R女性：17.5±1.0g；C女性：17.9±0.4g)。8周龄时，R公仔体重与C公仔无差异(R公仔175.5±4.3g，C公仔174.0±2.1g)。在8周龄时，R组雌性大鼠的收缩压、舒张压和平均血压均显著高于C组，而雄性大鼠仅R组的收缩压显著高于C组。在16周龄时，R组雌性大鼠的收缩压、舒张压和平均压均较C组升高，而雄性R组大鼠的收缩压和平均压较C组显著升高，心率无明显差异。Ne浓度依赖地刺激C和R子代的主动脉环张力，但差异不显著。L-NAME可显著刺激C代大鼠去甲肾上腺素的最大收缩，但对R代无明显作用。Valsartan显著抑制去甲肾上腺素(NE)引起的R子代主动脉收缩，但对C子代无明显抑制作用。结论：孕晚期严重营养不良可导致仔鼠短暂生长受限，成年后雌雄后代均可出现高血压。成人高血压的胎儿来源可能与性别有关，尤其是女性。胎儿来源的成人高血压可能是血管内皮功能障碍。

There was no difference in litter size between restricted (R) and Control (C) groups (R group (9.3±0.7, C group (10.6±0.7)). Body weight was significantly reduced in R offspring compared to C in both male and female offspring at day 1(R male ; 4.2±0.1g vs C male ; 5.2±0.1g, R female ; 4.1±0.1g vs C female ; 5.2±0.1g). Female body weight of R was no different to catch up from female offspring of C by only 2 weeks. (R female ; 17.5±1.0g vs C female ; 17.9±0.4g). However, male body weight of R was no different from male offspring of C by week 8 (R male ; 175.5±4.3g vs C male ; 174.0±2.1g. In 8 week offspring, systolic, diastolic and mean blood pressures (BP) were all significantly elevated in female rats of R compared with C. However, in male offspring, only systolic BP of R was significantly increased compared with C. Heart rate is not difference in C and R offspring. In 16 week offspring, systolic, diastolic and mean BP were all more elevated in female rats of R compared with C. In male offspring, systolic and mean BP of R was significantly increased compared with C. Heart rate was not difference in C and R male offspring. NE concentration-dependently stimulated tension of aortic rings from in C and R offspring, which was not significantly. Maximal contractions to NE were significantly stimulated by L-NAME in C, but not R offspring. Valsartan significantly inhibited aortic contractions by NE in R, but not C offspring. Conclusions : Severe under nutrition during late gestation in rats leads to transient growth restriction in the pups, induces hypertension in male and female offspring in adulthood. Fetal origin of adult hypertension might be gender-dependent, especially female. Fetal origin of adult hypertension might be vascular endothelial dysfunction.