1Department of Medicine, Jinan Central Hospital, Clinical Medical College of Shandong University, Jinan, Shandong, China and The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Shandong University, Qilu Hospital, Jinan, Shandong, China
The first two authors contributed equally to this work.
2The Second Hospital of Shandong University, Jinan, Shandong, China
3The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Shandong University, Qilu Hospital, Jinan, Shandong, China
4The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Shandong University, Qilu Hospital, Jinan, Shandong, China
5The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Shandong University, Qilu Hospital, Jinan, Shandong, China
6The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Shandong University, Qilu Hospital, Jinan, Shandong, China
7The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Shandong University, Qilu Hospital, Jinan, Shandong, China
8The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Shandong University, Qilu Hospital, Jinan, Shandong, China
Abstract
Background: Endothelial dysfunction plays a significant role in the pathogenesis of essential hypertension (EH). This trial was undertaken to reveal the effects of extended-release felodipine on endothelial vasoactive substances in EH patients.
Methods: A colorimetric chemical method was employed to measure the level of nitric oxide (NO) and nitric oxide synthase (NOS), while radioimmunoassay was employed to measure endothelin (ET), angiotensin-II (Ang-II), thromboxane A2 (TXA2) and prostacyclin I2 (PGI2) in plasma of the subjects. Group 1 consisted of 120 patients who were treated with a 4-week mono-therapy of felodipine. Group 2 consisted of 70 patients who were participating in fitness programs during this period. Another group comprising 80 individuals was selected as controls. Data from both the starting point and the ending point were collected and analyzed.
Results: After a 4-week mono-therapy of extended-release felodipine in Group 1, the levels of plasma ET, Ang-II and TXA2 decreased significantly, while levels of NO, NOS and PGI2 did not noticeably change. In Group 2, there were almost no changes in levels of ET, Ang-II, TXA2, NO, NOS and PGI2.
Conclusions: From these results, we conclude that felodipine reduced blood pressure by decreasing the secretion of ET, Ang-II and TXA2. Consequently, felodipine can revitalize the endothelial function in EH patients.
Clin Chem Lab Med 2008;46:393–5.
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