onr:"swepub:oai:gup.ub.gu.se/59553"
Sökning: onr:"swepub:oai:gup.ub.gu.se/59553" > Short-term administ...
- 1 av 1
- Föregående post
- Nästa post
- Till träfflistan
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)
- Gothenburg University,Göteborgs universitet,Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi,Institute of Physiology and Pharmacology, Dept of Physiology
-
- Klintland, Natalia, 1965 (författare)
- Gothenburg University,Göteborgs universitet,Hjärt-kärlinstitutionen,Cardiovascular Institute
-
- Caidahl, Kenneth, 1949 (författare)
- Karolinska Institutet,Gothenburg University,Göteborgs universitet,Hjärt-kärlinstitutionen,Cardiovascular Institute
- visa fler...
- visa färre...
- (creator_code:org_t)
- Springer Science and Business Media LLC, 2005
- 2005
- Engelska.
- Ingår i: BMC Physiol. - : Springer Science and Business Media LLC. - 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.
Nyckelord
- 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
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
- 1 av 1
- Föregående post
- Nästa post
- Till träfflistan
Hitta mer i SwePub
- Av författaren/redakt...
- Nyström, Henrik, ...
- Klintland, Natal ...
- Caidahl, Kenneth ...
- Bergström, Göran ...
- Wickman, Anna, 1 ...
- Artiklar i publikationen
- BMC Physiol
- Av lärosätet
- Göteborgs universitet
- Karolinska Institutet
Sök utanför SwePub
- Sök vidare i:
- Google Book Search
- Google Scholar
Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.
- Copyright © LIBRIS - Nationella bibliotekssystem
- LIBRIS.kb.se
