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Published on: May 10, 2022
Long-term circulatory consequences of perinatal iron deficiency in male Wistar rats
Stephane L Bourque1, Marina Komolova, Kanji Nakatsu
1Department of Pharmacology and Toxicology, Faculty of Health Sciences, Queen's University, Kingston, Ontario, Canada K7L 3N6.
Insights
Perinatal iron deficiency (PID) in rats leads to programmed cardiovascular complications, including altered blood pressure regulation in adulthood. The kidney
Area of Science:
- Perinatal nutrition
- Cardiovascular physiology
- Renal function
Background:
- Perinatal iron deficiency (PID) is linked to persistent cardiovascular abnormalities in offspring.
- The mechanisms underlying PID-induced hypertension, particularly the kidney's role, remain unclear.
Purpose of the Study:
- To investigate the circulatory complications of PID.
- To explore the role of the kidney in PID-related blood pressure dysregulation.
Main Methods:
- Female Wistar rats were fed low-iron or iron-enriched diets during gestation.
- Offspring blood pressure and renal hemodynamics were assessed in adulthood.
- Responses to sodium loading were evaluated in PID and control groups.
Main Results:
- Adult offspring of iron-deficient mothers exhibited elevated mean arterial and systolic pressures.
- The relationship between renal arterial and interstitial hydrostatic pressures was blunted in PID animals.
- PID offspring showed exaggerated blood pressure responses to altered sodium intake.
Conclusions:
- PID adversely affects blood pressure control in offspring.
- Altered intrarenal hemodynamic properties contribute to PID-induced hypertension.
- The kidney plays a significant role in the long-term cardiovascular consequences of perinatal iron deficiency.
Abstract:
Perinatal iron deficiency (PID) has been reported to induce developmental abnormalities, including cardiovascular complications in rats. These complications are believed to be "programmed" by an aberrant perinatal environment because the changes persist long after the insult is corrected (ie, despite subsequent iron replenishment). Little is known about the mechanisms by which PID affects blood pressure in the offspring, although the kidney is likely to play a central role. The objective of this study was to investigate the circulatory complications of PID and the putative role of the kidney involved therein. Before and throughout gestation, female Wistar rats were fed either a low-iron diet (3 ppm/10 ppm Fe) or an iron-enriched diet (225 ppm Fe). After giving birth, all of the dams were placed on a standard grain-based diet. At 24 hours postpartum, hematocrits and hemoglobin levels from offspring of iron-deficient mothers were 60% and 59% of control values, respectively. Adult PID animals had greater mean arterial pressures (110 versus 106 mm Hg) and systolic blood pressures (129 versus124 mm Hg) than controls, as assessed by radiotelemetry. The relationship between renal arterial pressure and renal interstitial hydrostatic pressure, assessed in anesthetized rats, was blunted by 41% in the PID group compared with controls. In addition, arterial pressure changes were significantly greater in response to altered sodium in the PID animals compared with controls. These data confirm that PID adversely affects blood pressure control, which seems to be mediated, at least in part, by altered intrarenal hemodynamic properties.
