title: Short-term treatment of spontaneously hypertensive rats with liver growth factor reduces carotid artery fibrosis, improves vascular function, and lowers blood pressure.
abstract: OBJECTIVE
  Liver growth factor (LGF), a mitogen for liver cells, reduces fibrosis in a rat model of cirrhosis. The present study assesses the possible vascular antifibrotic and antihypertensive effects of LGF treatment on spontaneously hypertensive rats (SHR).
  
  
  METHODS
  Six-month-old male SHR and normotensive Wistar Kyoto rats (WKY) were treated with LGF (4.5 microg LGF/rat i.p. twice a week for 2 weeks). Haemodynamic parameters were measured in anaesthetized rats. Vascular structure and function were studied in carotid arteries using optical and confocal microscopy, radioimmunoassay for desmosine, and isometric tension recording.
  
  
  RESULTS
  LGF reduced systolic and diastolic blood pressure only in SHR. When compared to those of untreated SHR, carotid arteries from LGF-treated SHR showed: 1) a 50% reduction in collagen area and an increase in vascular smooth muscle cell number in the media, 2) no difference in total elastin content, but an increase in size of fenestrae in the internal elastic lamina, and 3) enhanced relaxation to acetylcholine, sodium nitroprusside, and forskolin. These effects were specific for SHR, since no changes were observed in LGF-treated WKY.
  
  
  CONCLUSIONS
  Short-term treatment with a low dose of LGF induced a large improvement in vascular structure and function and significantly reduced blood pressure in a rat model of essential hypertension. The present results could open future research to explore the vascular effects of this endogenous factor in order to determine its potential as an antifibrotic and antihypertensive agent in humans.
authors.affiliation: Departamento de Fisiología, Facultad de Medicina, C/Arzobispo Morcillo 2, 28029 Madrid, Spain.
authors.forename: Beatriz
authors.initials: B
authors.lastname: Somoza
authors.forename: Fatima
authors.initials: F
authors.lastname: Abderrahim
authors.forename: José M
authors.initials: JM
authors.lastname: González
authors.forename: M Victoria
authors.initials: MV
authors.lastname: Conde
authors.forename: Silvia M
authors.initials: SM
authors.lastname: Arribas
authors.forename: Barry
authors.initials: B
authors.lastname: Starcher
authors.forename: Javier
authors.initials: J
authors.lastname: Regadera
authors.forename: María S
authors.initials: MS
authors.lastname: Fernández-Alfonso
authors.forename: Juan J
authors.initials: JJ
authors.lastname: Díaz-Gil
authors.forename: M Carmen
authors.initials: MC
authors.lastname: González
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001663:Bilirubin / Q000494:pharmacology*; D002339:Carotid Arteries / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D002452:Cell Count; D005576:Colforsin / Q000494:pharmacology; D003094:Collagen / Q000032:analysis; D003895:Desmosine / Q000032:analysis; D004305:Dose-Response Relationship, Drug; D004549:Elastin / Q000032:analysis; D005355:Fibrosis; D006973:Hypertension / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D066298:In Vitro Techniques; D007537:Isometric Contraction; D008297:Male; D018613:Microscopy, Confocal; D008934:Mitogens / Q000494:pharmacology*; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D032389:Myocytes, Smooth Muscle / Q000187:drug effects; D009599:Nitroprusside / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012709:Serum Albumin / Q000494:pharmacology*; D000075462:Serum Albumin, Human; D013997:Time Factors; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D008934:Mitogens; D012709:Serum Albumin; D014665:Vasodilator Agents; C053498:albumin-bilirubin complex; D003895:Desmosine; D009599:Nitroprusside; D005576:Colforsin; D003094:Collagen; D004549:Elastin; D000109:Acetylcholine; D001663:Bilirubin; D000075462:Serum Albumin, Human