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Acute vascular effects of vascular endothelial growth factor inhibition in the forearm arterial circulation.
Cameron, Alan C; Welsh, Paul; Neves, Karla B; Newby, David E; Touyz, Rhian M; Lang, Ninian N.
Afiliación
  • Cameron AC; BHF Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Science, University of Glasgow, Glasgow.
  • Welsh P; BHF Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Science, University of Glasgow, Glasgow.
  • Neves KB; BHF Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Science, University of Glasgow, Glasgow.
  • Newby DE; BHF Centre for Cardiovascular Sciences, University of Edinburgh, Edinburgh, UK.
  • Touyz RM; BHF Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Science, University of Glasgow, Glasgow.
  • Lang NN; BHF Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Science, University of Glasgow, Glasgow.
J Hypertens ; 38(2): 257-265, 2020 02.
Article en En | MEDLINE | ID: mdl-31449168
OBJECTIVE: Although vascular endothelial growth factor inhibition (VEGFi) represents a major therapeutic advance in oncology, it is associated with hypertension and adverse vascular thrombotic events. Our objective was to determine whether VEGFi caused direct vascular dysfunction through increased endothelin-1 (ET-1) activity or impaired endothelial vasomotor or fibrinolytic function. METHODS: Using forearm venous occlusion plethysmography, we measured forearm blood flow during intra-arterial infusions of bevacizumab (36-144 µg/dl forearm volume per minute) administered for 15-60 min in healthy volunteers (n = 6-8). On two separate occasions in 10 healthy volunteers, we further measured forearm blood flow and tissue plasminogen activator (t-PA) release during intra-arterial bradykinin infusion (100 and 1000 pmol/min) in the presence and absence of bevacizumab (144 µg/dl forearm volume per minute), and the presence and absence of endothelin A receptor antagonism with BQ-123 (10 nmol/min). Plasma t-PA and plasminogen activator inhibitor-1 (PAI-1) concentrations were measured at baseline and with each dose of bradykinin. RESULTS: Baseline blood flow and plasma ET-1, t-PA and PAI-1 concentrations were unaffected by bevacizumab. Bradykinin caused dose-dependent vasodilatation (P < 0.0001) and t-PA release (P < 0.01) but had no effect on plasma PAI-1 concentrations. Neither bevacizumab nor BQ-123 affected bradykinin-induced vasodilatation and t-PA release. CONCLUSION: Acute exposure to bevacizumab does not directly cause endothelial vasomotor or fibrinolytic dysfunction in healthy young volunteers.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Vasodilatación / Bevacizumab / Antebrazo / Antineoplásicos Inmunológicos Tipo de estudio: Clinical_trials Límite: Adult / Humans / Male / Middle aged Idioma: En Revista: J Hypertens Año: 2020 Tipo del documento: Article Pais de publicación: Países Bajos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Vasodilatación / Bevacizumab / Antebrazo / Antineoplásicos Inmunológicos Tipo de estudio: Clinical_trials Límite: Adult / Humans / Male / Middle aged Idioma: En Revista: J Hypertens Año: 2020 Tipo del documento: Article Pais de publicación: Países Bajos