title: Phenotype-related alteration in expression of natriuretic peptide receptors in aortic smooth muscle cells.
abstract: To elucidate the physiological and pathophysiological roles of the natriuretic peptide family in vascular smooth muscle cells, in which the natriuretic peptide family is implicated in growth inhibition as well as vasorelaxation, we have examined the phenotype-related expression of three kinds of natriuretic peptide receptors in rat aortic smooth muscle cells. The expression of natriuretic peptide receptors at the mRNA level was studied by Northern blot hybridization, and the expression at the protein level was determined by the cGMP production method and receptor binding assay. In intact aortic media, atrial natriuretic peptide (ANP)-A receptor mRNA and ANP-B receptor mRNA were detected, and the potency of cGMP production by ANP was at least two orders of magnitude stronger than that by C-type natriuretic peptide. Clearance receptor mRNA was undetectable, and only a small amount of the clearance receptor was detected by the binding assay in intact aortic media. By contrast, in cultured aortic smooth muscle cells at the first, fifth, and 17th passages, the ANP-B receptor mRNA level markedly increased; meanwhile, the expression of the ANP-A receptor mRNA became undetectable. C-type natriuretic peptide was one order of magnitude more potent than ANP in cGMP production in cultured aortic smooth muscle cells. The clearance receptor density and its mRNA level increased tremendously in these cultured cells. These results demonstrate that the marked phenotype-related alteration occurs in the expression of natriuretic peptide receptors in rat aortic smooth muscle cells.
authors.affiliation: Department of Medicine, Kyoto University School of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Suga
authors.forename: K
authors.initials: K
authors.lastname: Nakao
authors.forename: I
authors.initials: I
authors.lastname: Kishimoto
authors.forename: K
authors.initials: K
authors.lastname: Hosoda
authors.forename: M
authors.initials: M
authors.lastname: Mukoyama
authors.forename: H
authors.initials: H
authors.lastname: Arai
authors.forename: G
authors.initials: G
authors.lastname: Shirakami
authors.forename: Y
authors.initials: Y
authors.lastname: Ogawa
authors.forename: Y
authors.initials: Y
authors.lastname: Komatsu
authors.forename: O
authors.initials: O
authors.lastname: Nakagawa
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D001011:Aorta / Q000166:cytology / Q000378:metabolism*; D009320:Atrial Natriuretic Factor / Q000378:metabolism; D007536:Isomerism; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism*; D010641:Phenotype; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D017461:Receptors, Atrial Natriuretic Factor; D011956:Receptors, Cell Surface / Q000145:classification / Q000235:genetics / Q000378:metabolism*
chemical_list: D000199:Actins; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D009320:Atrial Natriuretic Factor; D017461:Receptors, Atrial Natriuretic Factor