This thesis investigates possible mechanisms underlying the decreased kidney size and the development of high blood pressure in the offspring of our model of maternal iron deficiency. This study has demonstrated that a maternal iron deficient diet has no effect on gene expression of either markers of vasculogenesis/angiogenesis or regulators of apoptosis and cell proliferation in the kidneys of the offspring. The effect of maternal iron deficiency on well documented mechanisms involved in blood pressure regulation were investigated in the offspring. The data showed that neither renal sodium transport nor nephron number are involved in hypertension development in our model of maternal iron deficiency. The renin angiotensin system showed significant increase in the renal renin mRNA expression, and pulmonary ACE1 mRNA and activity levels in newborn offspring of iron deficient mothers. These changes are unique for maternal iron deficiency as they have not been seen in the other models of nutritional programming. However, they are also temporary and disappear by two weeks after birth and at this stage it is unknown if and how the renin angiotensin system contributes to hypertension development in the offspring of iron deficient mothers. Finally, the whole rat genome arrays were used to identify new genes and pathways affected by maternal iron deficiency in fetal kidneys. The results of the microarray experiment suggested renal inflammation and increased collagen cross-linking leading to stiffening of vascular walls, as possible causes of hypertension in the offspring of iron deficient mothers. Further analysis showed, however, that both mechanisms do not appear to be involved. The microarray study also identified CD36 scavenger receptor as being significantly up-regulated in the kidneys of the fetuses of iron deficient mothers, but its expression significantly decreased in adult animals compared to controls. The data presented in this thesis indicate that the effect of an iron deficient diet on offspring blood pressure is multifactorial and complex.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:510538 |
| Date | January 2009 |
| Creators | Czopek, Alicja |
| Publisher | University of Aberdeen |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Source | http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=26459 |
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