Sex-specific response of renal Na,K-ATPase to prenatal angiotensin 2 exposure and increased salt intake in offspring.

In rodents, increased angiotensin 2 (Ang2) during pregnancy increases blood pressure and decreases salt sensitivity in the offspring. To explore the underlying mechanisms, this study evaluated the effects of prenatal Ang2 exposure on the activity of renal Na,K-ATPase, which is one of the main systems that maintains sodium ion homeostasis in an organism. Moreover, this study also investigated the impact of a higher-salt diet on the enzyme activity in the offspring in a sex-dependent manner. Pregnant Wistar rats were implanted with osmotic minipumps that continuously released Ang2 (2 μg/kg/h) for 2 weeks. Male and female offspring of treated and control females were allocated to groups fed with normal or high-salt diets. In the offspring prenatally treated with Ang2, a significant V_max increase (23 - 36%) was observed in females fed with both a normal and high-salt diet. In addition, a significant increase in K_m (20 - 26%) was also observed in the female groups, compared to respective male groups, independently of their diet. Evaluation of K_Na showed significantly lower values (13 - 17%) in female offspring fed with a high-salt diet, independent of the prenatal treatment. In conclusion, these data suggest that increased prenatal Ang2 has a predominant impact on the properties of renal Na,K-ATPase in both sexes. Moreover, the enzyme is resistant to higher salt intake in offspring prenatally exposed to Ang2.

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