title: Modulation of vascular natriuretic peptide receptor gene expression in hypertensive and obese hyperglycemic rats.
abstract: Receptors for natriuretic peptide (NP) consist of three subtypes: NP-A, NP-B, and NP-C. Recent studies in cultured aortic cells have suggested a phenotype-related switching of the vascular NP receptor from NP-A to NP-B. To ascertain the biological significance of the phenomenon in vivo, we developed a sensitive and reproducible ribonuclease protection assay and determined each receptor messenger RNA (mRNA) level in the vascular vessels of stroke-prone spontaneously hypertensive rats, deoxycorticosterone acetate-salt hypertensive rats, and genetically hyperglycemic. Wistar fatty rats and in cultured aortic smooth muscle cells. The aortic NP-A receptor mRNA level was significantly up-regulated in both types of hypertensive rats, whereas the NP-B receptor mRNA level did not show any significant change. Both NP-A and NP-B receptor mRNA levels were significantly up-regulated in Wistar fatty rats compared with the control values. There was no significant up-regulation of NP-A receptor mRNA in the inferior vena cava of the stroke-prone spontaneously hypertensive rats. Although the NP-A receptor was always the predominant subtype in rat aortic tissue, NP-B receptor was the predominant subtype in aortic smooth muscle cells in culture. These findings suggest that up-regulation of the NP-A receptor, but not the subtype switching, is the major modulation of receptor gene expression in both hypertensive and diabetic rats.
authors.affiliation: Department of Medicine, Tokyo Women's Medical College, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Yoshimoto
authors.forename: M
authors.initials: M
authors.lastname: Naruse
authors.forename: K
authors.initials: K
authors.lastname: Naruse
authors.forename: Y
authors.initials: Y
authors.lastname: Fujimaki
authors.forename: A
authors.initials: A
authors.lastname: Tanabe
authors.forename: T
authors.initials: T
authors.lastname: Muraki
authors.forename: M
authors.initials: M
authors.lastname: Itakura
authors.forename: H
authors.initials: H
authors.lastname: Hagiwara
authors.forename: S
authors.initials: S
authors.lastname: Hirose
authors.forename: H
authors.initials: H
authors.lastname: Demura
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000378:metabolism; D001483:Base Sequence; D002478:Cells, Cultured; D017931:DNA Primers / Q000235:genetics; D015870:Gene Expression; D006162:Guanylate Cyclase / Q000235:genetics; D006943:Hyperglycemia / Q000235:genetics / Q000378:metabolism; D006973:Hypertension / Q000235:genetics* / Q000378:metabolism; D008297:Male; D008969:Molecular Sequence Data; D009131:Muscle, Smooth, Vascular / Q000378:metabolism; D009765:Obesity / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D017461:Receptors, Atrial Natriuretic Factor / Q000235:genetics*; D018000:Receptors, Peptide / Q000145:classification / Q000235:genetics*; D012260:Ribonucleases; D015854:Up-Regulation; D014682:Vena Cava, Inferior / Q000378:metabolism
chemical_list: D017931:DNA Primers; D012333:RNA, Messenger; D018000:Receptors, Peptide; D012260:Ribonucleases; D006162:Guanylate Cyclase; D017461:Receptors, Atrial Natriuretic Factor; C073616:atrial natriuretic factor receptor C