title: Induction of growth hormone receptor and insulin-like growth factor-I mRNA in aorta and caval vein during hemodynamic challenge.
abstract: Induction of two-kidney, one clip hypertension (renal hypertension) is characterized by a slow increase in left ventricular tension and aortic wall stress, as opposed to aortocaval fistula or shunt volume overload, which induces a marked and rapid onset of wall stress in the caval vein and right ventricle. In the present study, we applied hemodynamic challenge to study the growth response involving gene expression of insulin-like growth factor-I (IGF-I) and growth hormone receptor (GH-R) mRNA in aorta and caval vein. Volume overload and pressure overload were induced in Wistar rats by means of shunt and renal hypertension, respectively. Systolic pressure was measured before excision of the great vessels, which was performed between 2 and 12 days postoperatively. Aortic and caval vein IGF-I and GH-R mRNA expressions were measured by means of a solution hybridization assay, and the caval vein was analyzed for IGF-I protein by immunohistochemistry. In the volume-distended but not pressurized caval vein in shunt rats, verified by telemetry recordings, there was an eightfold increase in IGF-I and 3.5-fold increase in GH-R mRNA at day 4 versus control. The IGF-I protein appeared to be localized in smooth muscle cells. In the aorta of the renal hypertension group, changes were of a slower onset. At day 7, there was a fourfold increase in IGF-I and five-fold increase of GH-R mRNA expressions versus sham-operated rats. Both the shunt caval vein and renal hypertension aorta showed evidence of a structural adaptation of the growth response. The present study suggests that acute elevation in vascular wall stress is an important triggering factor for overexpression of IGF-I and GH-R mRNA in great vessels. The growth hormone/insulin-like growth factor axis may be an important link in mediating structurally adaptive growth responses in the blood vessel wall.
authors.affiliation: Department of Physiology, University of Göteborg, Sweden.
authors.forename: A
authors.initials: A
authors.lastname: Wickman
authors.forename: P
authors.initials: P
authors.lastname: Friberg
authors.forename: M A
authors.initials: MA
authors.lastname: Adams
authors.forename: G L
authors.initials: GL
authors.lastname: Matejka
authors.forename: C
authors.initials: C
authors.lastname: Brantsing
authors.forename: G
authors.initials: G
authors.lastname: Guron
authors.forename: J
authors.initials: J
authors.lastname: Isgaard
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism* / Q000601:surgery; D001166:Arteriovenous Shunt, Surgical / Q000009:adverse effects; D005786:Gene Expression Regulation; D006439:Hemodynamics; D006973:Hypertension / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D006977:Hypertension, Renal / Q000378:metabolism / Q000503:physiopathology; D007150:Immunohistochemistry; D008297:Male; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D051381:Rats; D017208:Rats, Wistar; D017526:Receptor, IGF Type 1 / Q000032:analysis / Q000096:biosynthesis / Q000235:genetics*; D011986:Receptors, Somatotropin / Q000032:analysis / Q000096:biosynthesis / Q000235:genetics*; D012260:Ribonucleases / Q000235:genetics; D014684:Venae Cavae / Q000378:metabolism* / Q000601:surgery
chemical_list: D012333:RNA, Messenger; D011986:Receptors, Somatotropin; D017526:Receptor, IGF Type 1; D012260:Ribonucleases