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Short-term administration of growth hormone (GH) lowers blood pressure by activating eNOS/nitric oxide (NO)-pathway in male hypophysectomized (Hx) rats

Nyström, Henrik, 1977- (författare)
Göteborgs universitet, Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi
Klintland, Natalia, 1965- (författare)
Göteborgs universitet, Hjärt-kärlinstitutionen
Caidahl, Kenneth, 1949- (författare)
Göteborgs universitet, Hjärt-kärlinstitutionen
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Bergström, Göran, 1964- (författare)
Göteborgs universitet, Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi
Wickman, Anna, 1969- (författare)
Göteborgs universitet, Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi
visa färre...
Göteborgs universitet Sahlgrenska akademin. Hjärt-kärlinstitutionen. 
Göteborgs universitet Sahlgrenska akademin. Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi. 
2005
Engelska.
Ingår i: BMC Physiol. - 1472-6793. ; 5
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • BACKGROUND: The aim of the study was to evaluate the acute and continuous (up to 14 days of treatment) effect of growth hormone (GH) on blood pressure (BP) regulation and to investigate the interplay between GH, nitric oxide (NO) and BP. In un-supplemented and GH supplemented hypophysectomized (Hx) male rats as well as intact rats, continuous resting mean arterial blood pressure (MAP) was measured using telemetry. Baroreceptor activity and the influences of NO on BP control were assessed during telemetric measurement. Furthermore, basal plasma and urine nitrate levels and aortic endothelial nitric oxide synthase (eNOS) expression were analysed. Endothelial function as well as vascular structure in the hindquarter vascular bed was estimated using an in vivo constant-flow preparation. RESULTS: Hypophysectomy was associated with decreased MAP (Hx: 83 +/- 3 vs Intact: 98 +/- 6 mmHg, p < 0.05) and heart rate (HR) (Hx: 291 +/- 4 vs Intact: 351 +/- 7 beat/min, p < 0.05). Endothelial dysfunction and reduced vasculature mass in the hindquarter vascular bed was found in Hx rats. GH substitution caused a further transient decrease in MAP and a transient increase in HR (14% and 16% respectively, p < 0.05). The reduction in MAP appeared to be NO dependent. Aortic eNOS expression was unchanged. GH substitution resulted in an impaired baroreceptor function. Two weeks of GH treatment did not normalise the BP, vascular structure and the endothelial function in the resistance vessels. CONCLUSION: GH substitution seems to have a short lasting effect on lowering blood pressure via activation of the NO-system. An interaction between GH, NO-system and BP regulation can be demonstrated.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  (hsv//swe)
MEDICAL AND HEALTH SCIENCES  (hsv//eng)

Nyckelord

MEDICIN
MEDICINE
Animals
Blood Pressure/*drug effects/physiology
Blood Vessels/drug effects/physiology
Body Weight/drug effects
Drug Administration Schedule
Enzyme Activation/drug effects
Enzyme Inhibitors/pharmacology
Growth Hormone/*administration & dosage/pharmacology
Heart/anatomy & histology
Heart Rate/drug effects
*Hypophysectomy
Insulin-Like Growth Factor I/metabolism
Male
Muscle
Skeletal/blood supply
NG-Nitroarginine Methyl Ester/pharmacology
Nitrates/blood/urine
Nitric Oxide/*metabolism
Nitric Oxide Synthase Type III/*metabolism
Organ Size/drug effects
Pressoreceptors/drug effects
Rats
Rats
Wistar
Vascular Resistance

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