201. Maternal Iron Deficiency Programs Rat Offspring Hypertension in Relation to Renin—Angiotensin System and Oxidative Stress.
- Author
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Chang, Ya-Hui, Chen, Wan-Hsuan, Su, Chung-Hao, Yu, Hong-Ren, Tain, You-Lin, Huang, Li-Tung, and Sheen, Jiunn-Ming
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IRON deficiency , *OXIDATIVE stress , *RENIN-angiotensin system , *ANGIOTENSINS , *RENIN , *KIDNEY cortex , *ANGIOTENSIN converting enzyme - 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. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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