Alteration of endothelium-mediated vasodilator response in the rat hindlimb vasculature consecutive to chronic hypoxic stress: NO and EDHF involvement

Autor: Cyril Reboul, Michel Dauzat, Stéphane Tanguy, Philippe Obert, A. Gibault
Přispěvatelé: Physiopathologie des adaptations cardiovasculaires à l'Exercice, Avignon Université (AU), Caractéristiques féminines des dysfonctions des interfaces cardio-vasculaires (EA 2992), Université Montpellier 1 (UM1)-Université de Montpellier (UM)
Jazyk: angličtina
Rok vydání: 2009
Předmět:
Male
Time Factors
Physiology
MESH: Random Allocation
Blood Pressure
Vasodilation
Hindlimb
030204 cardiovascular system & hematology
Biological Factors
Random Allocation
chemistry.chemical_compound
0302 clinical medicine
MESH: Animals
Infusions
Intravenous
MESH: Stress
Physiological
MESH: Hindlimb
MESH: Arginine
MESH: Blood Pressure
medicine.anatomical_structure
Anesthesia
cardiovascular system
Molecular Medicine
MESH: Nitric Oxide Synthase
MESH: Endothelium
Vascular
Acetylcholine
MESH: Oxygen
medicine.drug
Atmosphere Exposure Chambers
medicine.medical_specialty
Endothelium
MESH: Rats
MESH: Atmosphere Exposure Chambers
Hypoxic stress
Arginine
Nitric Oxide
Apamin
Nitric oxide
MESH: Vasodilation
03 medical and health sciences
MESH: Diet
[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system
Stress
Physiological
EDHF
Internal medicine
medicine
Animals
MESH: Infusions
Intravenous
Pharmacology
business.industry
MESH: Acetylcholine
MESH: Time Factors
NO pathway
Blood flow
Vascular function
MESH: Male
Diet
Rats
Oxygen
Endocrinology
Blood pressure
chemistry
Regional Blood Flow
MESH: Nitric Oxide
MESH: Biological Factors
MESH: Regional Blood Flow
Endothelium
Vascular
Nitric Oxide Synthase
business
030217 neurology & neurosurgery
Zdroj: Vascular Pharmacology
Vascular Pharmacology, Elsevier, 2009, 51 (2-3), pp.154-61. ⟨10.1016/j.vph.2009.05.004⟩
ISSN: 1537-1891
DOI: 10.1016/j.vph.2009.05.004⟩
Popis: International audience; The previously documented impairment of hindlimb blood flow consecutive to chronic hypoxia might be related to endothelial vasomotor dysfunction. The aim of this study was to assess in-vivo the effect of chronic hypoxic stress on endothelium-mediated vasodilator response of hindlimb vascular bed, especially as regards to endothelium-derived hyperpolarizing factor (EDHF) and nitric oxide (NO) pathway contribution. Dark Agouti rats were randomly assigned to live at barometric pressure approximately 760 mmHg (N rats) or approximately 550 mmHg (CH rats). Under anesthesia, catheters were placed in the carotid artery for arterial pressure measurement, and in the saphenous vein and iliac artery for drug delivery. Hindlimb blood flow (HBF) was measured by transit-time ultrasound flowmetry, at baseline and during endothelium-dependent vasodilator response induced by intra-arterial injection of acetylcholine (0.75 ng and 7.5 ng) with and without specific blockers of NOS (L-NAME) and EDHF (Charybdotoxin+Apamin). HBF and hindlimb vascular conductance changes in response to ACh infusion were significantly lower in CH than in N rats. The mechanisms responsible for this blunted response involved impairment in both NO pathway and EDHF. The chronic hypoxia-induced alteration of NO pathway was mainly related to the bioavailability of its substrate l-Arginine, since the infusion of l-Arginine restored the endothelial response to ACh in CH rats to the level of N rats. These results demonstrate that the impairment in endothelium-mediated vasodilator response of the hindlimb vascular tree induced by chronic hypoxic stress involves both NO and EDHF.
Databáze: OpenAIRE
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