Journal
PHARMACOLOGY RESEARCH & PERSPECTIVES
Volume 10, Issue 4, Pages -Publisher
JOHN WILEY & SONS LTD
DOI: 10.1002/prp2.991
Keywords
bone tissue; hepatic; hypertension; iron metabolism; Prazosin
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Funding
- National Natural Science Foundation of China [31340064]
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The relationship between cardiovascular diseases and iron disorders has gained attention. This study found that treatment with the hypotensive drug prazosin can affect iron metabolism in spontaneously hypertensive rats, leading to changes in iron levels in the serum, liver, and bone tissue. These findings indicate that hypertension and anti-hypertensive drugs can impact iron homeostasis, and there may be different iron regulatory mechanisms between hypertensive and normal animals.
The relationship between cardiovascular diseases and iron disorders has gained increasing attention; however, the effects of hypotensive drugs on iron metabolic alterations in hypertension are not well understood. The purpose of this study was to investigate iron metabolic changes after prazosin treatment of spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats. Our second objective was to examine the effects of hypertension and anti-hypertensive drugs on bone formation and resorption. SHRs and WKY rats were randomized into either prazosin-treated groups (WKY+ PZ and SHR + PZ) or untreated groups (WKY and SHR). After 7days of intragastric prazosin administration, the rats were sacrificed for analysis; blood samples and organs (the duodenum, liver, kidneys, spleen, and femur) were collected. Both WKY+ PZ and SHR groups exhibited iron deficiency in the serum and liver. Prazosin increased the iron levels in the bone tissue of SHRs. Prazosin stimulated the expression of hepcidin mRNA in the liver of SHRs and inhibited the expression of this iron-regulatory hormone in WKY rats. FPN1 expression in the duodenum was increased significantly in SHRs, however markedly decreased after prazosin treatment. The expression of TLR4 and Ctsk was enhanced in the bone tissue of SHRs, whereas CLC-7 expression was inhibited. Both hypotension and hypertension can lead to iron deficiency. Treatment with prazosin restored iron homeostasis in SHRs. The inverse impacts of prazosin on hepatic hepcidin expression in SHRs versus WKY rats indicates differing iron regulatory mechanisms between hypertensive and normal animals. The osteoclast activity was found to be enhanced in SHRs. Further study is needed to address whether the changes in osteoblast and osteoclast activity in SHRs correlates with the effects on iron metabolism.
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