Academic Journal
Effects of adrenomedullin, C-type natriuretic peptide, and parathyroid hormone-related peptide on calcification in cultured rat vascular smooth muscle cells
العنوان: | Effects of adrenomedullin, C-type natriuretic peptide, and parathyroid hormone-related peptide on calcification in cultured rat vascular smooth muscle cells |
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المؤلفون: | Huang, ZY, Li, JX, Jiang, ZS, Qi, YF, Tang, CS, Du, JB |
المساهمون: | Tang, CS (reprint author), Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100083, Peoples R China., Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100083, Peoples R China., Peking Univ, Hosp 1, Dept Pediat, Beijing 100083, Peoples R China. |
المصدر: | SCI ; PubMed |
بيانات النشر: | journal of cardiovascular pharmacology |
سنة النشر: | 2003 |
المجموعة: | Peking University Institutional Repository (PKU IR) / 北京大学机构知识库 |
مصطلحات موضوعية: | vascular calcification, vascular smooth muscle cells, adrenomedullin, C-type natriuretic peptide, parathyroid hormone, ARTERIAL CALCIFICATION, OSTEOBLASTIC DIFFERENTIATION, OSTEOPONTIN, INHIBITION, GENE |
الوصف: | To clarify the regulating mechanism of vascular calcification, the investigators observed the effects of three vasoactive peptides, adrenomedullin (ADM), C-type natriuretic peptide (CNP), and parathyroid hormone-related peptide (PTHrP) on calcification in rat vascular smooth muscle cells (VSMCs). Beta-glycerophosphate stimulated growth and calcification in VSMCs. Adrenomedullin and CNP lowered beta-glycerophosphate-induced increase in VSMC growth. All three vasoactive peptides attenuated the increases of Ca-45 accumulation, calcium content, and alkaline phosphatase activity in calcified VSMCs. As for comparing the inhibitory effects, the strongest was PTHrP. Both ADM and PTHrP increased cyclic adenosine monophosphate (cAMP) content in calcified VSMCs, but CNP up-regulated cyclic guanosine monophosphate (cGMP) content. The PKA inhibitor PKAI completely reversed the inhibition of ADM on cell growth and all inhibitory effects of PTHrP on the parameters of calcification. The PKG inhibitor H8, however, strongly antagonized all the inhibitory effects of CNP on calcification. These data suggested that beta-glycerophosphate-induced calcification in VSMCs was inhibited by ADM, CNP, and PTHrP. Adrenomedullin and PTHrP inhibited VSMC calcification partially through the cAMP/PKA pathway, whereas CNP inhibited VSMC calcification through the cGMP/PKG pathway. This study could be of help in understanding the pathogenesis of vascular calcification, and providing new target for clinical treatment of cardiovascular diseases associated with vascular calcification. ; Cardiac & Cardiovascular Systems ; Pharmacology & Pharmacy ; SCI(E) ; PubMed ; 27 ; ARTICLE ; 1 ; 89-97 ; 42 |
نوع الوثيقة: | journal/newspaper |
اللغة: | English |
تدمد: | 0160-2446 |
Relation: | JOURNAL OF CARDIOVASCULAR PHARMACOLOGY.2003,42,(1),89-97.; 678353; http://hdl.handle.net/20.500.11897/346625; WOS:000183897600014 |
DOI: | 10.1097/00005344-200307000-00014 |
الاتاحة: | https://hdl.handle.net/20.500.11897/346625 https://doi.org/10.1097/00005344-200307000-00014 |
رقم الانضمام: | edsbas.674E63F0 |
قاعدة البيانات: | BASE |
تدمد: | 01602446 |
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DOI: | 10.1097/00005344-200307000-00014 |