Faculty, Staff and Student Publications

Publication Date

7-27-2022

Journal

International Journal of Molecular Sciences

Abstract

Hypertension is an important public health challenge, affecting up to 30-50% of adults worldwide. Several epidemiological studies indicate that high blood pressure originates in fetal life-the so-called programming effect or developmental origin of hypertension. Iron-deficiency anemia has become one of the most prevalent nutritional problems globally. Previous animal experiments have shown that prenatal iron-deficiency anemia adversely affects offspring hypertension. However, the underlying mechanism remains unclear. We used a maternal low-iron diet Sprague Dawley rat model to study changes in blood pressure, the renal renin-angiotensin system, oxidative stress, inflammation, and sodium transporters in adult male offspring. Our study revealed that 16-week-old male offspring born to mothers with low dietary iron throughout pregnancy and the lactation period had (1) higher blood pressure, (2) increased renal cortex angiotensin II receptor type 1 and angiotensin-converting enzyme abundance, (3) decreased renal cortex angiotensin II receptor type 2 and MAS abundance, and (4) increased renal 8-hydroxy-2'-deoxyguanosine and interleukin-6 abundance. Improving the iron status of pregnant mothers could influence the development of hypertension in their offspring.

Keywords

Anemia, Iron-Deficiency, Animals, Blood Pressure, Female, Hypertension, Iron, Iron Deficiencies, Iron, Dietary, Kidney, Lactation, Male, Maternal Nutritional Physiological Phenomena, Oxidative Stress, Pregnancy, Prenatal Exposure Delayed Effects, Rats, Rats, Sprague-Dawley, Receptors, Angiotensin, Renin-Angiotensin System

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