title: Endogenous aldosterone is involved in vascular calcification in rat.
abstract: Aldosterone (Aldo) is an important active hormone in the renin-angiotensin-aldosterone system and plays a vital role in the development of hypertension, heart failure and other cardiovascular diseases. We aimed to explore the role of endogenous Aldo in aortic calcification in rats. We induced arterial calcification in rats by intramuscular administration of vitamin D(3) plus oral nicotine (VDN) and determined calcium content, (45)Ca(2+) accumulation and activity of alkaline phosphatase (ALP). The mRNA level of osteopontin (OPN) was measured by semi-quantitative reverse transcriptase polymerase chain reaction. Deposition of collagen in the aorta wall was measured by Sirius red staining. The content of angiotensin II (Ang II) and Aldo in plasma and myocardial and vascular tissue was determined by radioimmunoassay. In rats with VDN treatment, von Kossa staining showed calcification in vascular smooth muscle cells and extracellular matrix, and the content of calcium in calcified arteries was 5.8-fold of that in control arteries (P < 0.01). The accumulation of (45)Ca(2+) and activity of ALP in calcified aortic tissue was three- and 2.5-fold, respectively, that in control tissue (P < 0.01). The mRNA expression of OPN was significantly higher, by 58%, in calcified than control tissue (P < 0.01). Vascular fibrosis was greater in rats with calcified tissue than in control rats. The level of Ang II and Aldo was 58% and 80% higher, respectively, in calcified than control tissue (both P < 0.01). The changes could be significantly improved by treatment with captopril, an angiotensin-converting enzyme inhibitor, and the Aldo receptor antagonist spironolactone. These results suggest that Aldo is an endogenous bioactive factor involved in vascular calcification.
authors.affiliation: Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Peking University Health Science Center, Beijing 100191, China.
authors.forename: Sheng-Ying
authors.initials: SY
authors.lastname: Wu
authors.forename: Yan-Rong
authors.initials: YR
authors.lastname: Yu
authors.forename: Yan
authors.initials: Y
authors.lastname: Cai
authors.forename: Li-Xin
authors.initials: LX
authors.lastname: Jia
authors.forename: Xiong
authors.initials: X
authors.lastname: Wang
authors.forename: Chuan-Shi
authors.initials: CS
authors.lastname: Xiao
authors.forename: Chao-Shu
authors.initials: CS
authors.lastname: Tang
authors.forename: Yong-Fen
authors.initials: YF
authors.lastname: Qi
mesh_terms: D000450:Aldosterone / Q000097:blood / Q000378:metabolism*; D000469:Alkaline Phosphatase / Q000378:metabolism; D000804:Angiotensin II / Q000032:analysis / Q000097:blood; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use; D000818:Animals; D001011:Aorta / Q000737:chemistry; D002118:Calcium / Q000032:analysis*; D002216:Captopril / Q000008:administration & dosage / Q000627:therapeutic use; D002762:Cholecalciferol; D003094:Collagen / Q000378:metabolism; D005355:Fibrosis; D006973:Hypertension / Q000378:metabolism; D008297:Male; D000451:Mineralocorticoid Receptor Antagonists / Q000008:administration & dosage / Q000627:therapeutic use; D009538:Nicotine; D053495:Osteopontin / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013148:Spironolactone / Q000008:administration & dosage / Q000627:therapeutic use; D061205:Vascular Calcification / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000451:Mineralocorticoid Receptor Antagonists; D012333:RNA, Messenger; D053495:Osteopontin; D000804:Angiotensin II; D002762:Cholecalciferol; D013148:Spironolactone; D000450:Aldosterone; D009538:Nicotine; D003094:Collagen; D002216:Captopril; D000469:Alkaline Phosphatase; D002118:Calcium