title: GH and IGF-I regulate the expression of endothelial nitric oxide synthase (eNOS) in cardiovascular tissues of hypophysectomized female rats.
abstract: OBJECTIVE
  This study explored whether short-term replacement therapy with growth hormone (GH) affects blood pressure (BP), heart rate (HR) and endothelial nitric oxide synthase (eNOS) expression in cardiovascular tissues in hypophysectomized (Hx) female rats.
  
  
  METHODS
  BP, HR and the expression of eNOS in the aorta, caval vein and heart were studied in Hx female rats and in Hx female rats that underwent 7 days treatment with GH and thyroxine+glucocorticoids ([T(4)+GC]). Insulin-like growth factor-I (IGF-I) was included in a second experimental protocol to explore the indirect effect of GH. The expression and localisation of eNOS was analysed by immunoblotting and immunohistochemistry.
  
  
  RESULTS
  Decreased BP (Hx 98+/-1, Intact 129+/-3 mmHg, P<0.05), HR (Hx 297+/-14, Intact 399+/-31 beats/min, P<0.05) and unchanged eNOS expression was demonstrated in Hx compared with intact rats. None of the hormones affected BP, but both GH and IGF-I increased HR compared with Hx rats (GH 358+/-10, IGF-I 337+/-7, Hx 306+/-11 beats/min, P<0.05). Replacement of GH, GH+[T(4)+GC] and IGF-I resulted in an increased aortic eNOS expression (GH 161+/-24, GH+[T(4)+GC] 177+/-25, IGF-I 153+/-21, Hx 109+/-7%, P<0.05), whereas in caval vein only GH+[T(4)+GC] affected eNOS expression. None of the hormones changed the level of eNOS in the heart. eNOS was localised in the intima layer of the aorta, whereas in the caval vein eNOS was localised in all cell layers.
  
  
  CONCLUSIONS
  These findings support the suggested positive role of GH in the regulation of the cardiovascular homeostasis. The observed up-regulation of eNOS, and presumably an increased NO bioavailability, may result in improved endothelial and cardiovascular function.
authors.affiliation: Department of Physiology, Goteborg University, PO Box 432, Goteborg S-405 30, Sweden. anna.wickman@fysiologi.gu.se
authors.forename: Anna
authors.initials: A
authors.lastname: Wickman
authors.forename: Ingibjorg H
authors.initials: IH
authors.lastname: Jonsdottir
authors.forename: Goran
authors.initials: G
authors.lastname: Bergstrom
authors.forename: Lars
authors.initials: L
authors.lastname: Hedin
mesh_terms: D000199:Actins / Q000032:analysis; D000818:Animals; D001011:Aorta / Q000737:chemistry / Q000201:enzymology*; D001794:Blood Pressure; D001835:Body Weight; D003243:Consciousness; D005260:Female; D013006:Growth Hormone / Q000494:pharmacology*; D006339:Heart Rate; D007016:Hypophysectomy; D007334:Insulin-Like Growth Factor I / Q000378:metabolism / Q000494:pharmacology*; D009206:Myocardium / Q000737:chemistry / Q000201:enzymology* / Q000473:pathology; D019001:Nitric Oxide Synthase / Q000032:analysis / Q000096:biosynthesis*; D052250:Nitric Oxide Synthase Type III; D009929:Organ Size; D051381:Rats; D017208:Rats, Wistar; D014682:Vena Cava, Inferior / Q000737:chemistry / Q000201:enzymology; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D000199:Actins; D014841:von Willebrand Factor; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat