Abstract
BackgroundMaternal protein restriction during rat pregnancy is known to impact upon fetal development, growth and risk of disease in later life. It is of interest to understand how protein undernutrition influences the normal maternal adaptation to pregnancy. Here we investigated the mechanisms regulating renal haemodynamics and plasma volume during pregnancy, in the context of both normal and reduced plasma volume expansion. The study focused on expression of renal angiotensin receptors (ATR) and vasopressin-related aquaporins (AQP), hypothesising that an alteration in the balance of these proteins would be associated with pregnancy per se and with compromised plasma volume expansion in rats fed a low-protein diet.MethodsFemale Wistar rats were mated and fed a control (18% casein) or low-protein (9% casein) diet during pregnancy. Animals were anaesthetised on days 5, 10, 15 and 20 of gestation (n = 8/group/time-point) for determination of plasma volume using Evans Blue dye, prior to euthanasia and collection of tissues. Expression of the ATR subtypes and AQP2, 3 and 4 were assessed in maternal kidneys by PCR and western blotting. 24 non-pregnant Wistar rats underwent the same procedure at defined points of the oestrous cycle.ResultsAs expected, pregnancy was associated with an increase in blood volume and haemodilution impacted upon red blood cell counts and haemoglobin concentrations. Expression of angiotensin II receptors and aquaporins 2, 3 and 4 was stable across all stages of the oestrus cycle. Interesting patterns of intra-renal protein expression were observed in response to pregnancy, including a significant down-regulation of AQP2. In contrast to previous literature and despite an apparent delay in blood volume expansion in low-protein fed rats, blood volume did not differ significantly between groups of pregnant animals. However, a significant down-regulation of AT2R protein expression was observed in low-protein fed animals alongside a decrease in creatinine clearance.ConclusionRegulatory systems involved in the pregnancy-induced plasma volume expansion are susceptible to the effects of maternal protein restriction.
Highlights
Maternal protein restriction during rat pregnancy is known to impact upon fetal development, growth and risk of disease in later life
The events leading to plasma volume expansion are not fully understood, but evidence suggests that it is triggered by a fall in systemic vascular tone [6]
The plasma volume expansion is associated with a substantial increase in effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) from as early as the sixth week of human pregnancy [9,10]
Summary
Maternal protein restriction during rat pregnancy is known to impact upon fetal development, growth and risk of disease in later life. The events leading to plasma volume expansion are not fully understood, but evidence suggests that it is triggered by a fall in systemic vascular tone [6]. This is thought to be followed by compensatory activation of volume-restoring mechanisms, including activation of the renin-angiotensin-aldosterone (RAAS) and argininevasopressin (AVP) systems [7,8], leading to renal sodium and water retention. The plasma volume expansion is associated with a substantial increase in effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) from as early as the sixth week of human pregnancy [9,10]. A role for the fetoplacental compartment has been suggested, based on fetal reduction experiments in rodents [13] and the greater volume expansion observed in human twin pregnancies [14]
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