Conference Paper

Exposure of pregnant rats to angiotensin 2 leads to an increase in blood pressure in their adult male offspring

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Renin-angiotensin-aldosterone system (RAAS) has an essential role in the homeostatic control of arterial blood pressure (BP), in tissue perfusion and control of extracellular fluid volume. Some pathological conditions such as preeclampsia or gestational diabetes mellitus may lead to increased activity of certain pathways the RAAS during pregnancy and modulate the development of key organs in regulating blood pressure. The aim of our experiment was to evaluate the effect of increased angiotensin 2 (Ang2), as a key hormone of RAAS, during pregnancy of female Wistar rats on BP of their offspring and sensitivity to salt intake in adulthood. Experimental females (n = 5) were on 6th day of gestation implanted with osmotic minipumps releasing Ang2 (2 mg×kg-1×h-1) and control females (n = 4) were sham-operated at the same time. For analysis, we used their offspring, 14 males affected by prenatal Ang2 (A) and 12 control (C) males. We measured BP using tail cuff plathysmography method and determined plasma renin activity (PRA), aldosterone, triiodothyronine (T3) and thyroxine (T4) levels by radioimmunoassay in their plasma. Fixated kidneys were frozen and used for morphological and immunohistochemical analyses. Prenatal exposure to Ang2 led to increase in BP in adult male rats, with no effect of increased salt (2% NaCl) intake. Relative heart weight did not change between the groups, but we observed a tendency to increase in the relative weight of the kidneys in C rats fed with 2% NaCl. Aldosterone levels did not change between A and C males, however we observed in both groups a decline as an effect of higher concentrations of salt in their diet. In PRA, we observed a decline after applying salt only in A rats. Our results demonstrate an organizational impact of a prenatal exposure to Ang2 on increase in BP and suggest the role of early ontogeny for the setup of BP regulation.

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