Vascular endothelial growth factor inhibitor-induced
hypertension: from pathophysiology to prevention and treatment
based on long-acting nitric oxide donors.

J 2014

Vascular endothelial growth factor inhibitor-induced hypertension: from pathophysiology to prevention and treatment based on long-acting nitric oxide donors.

KRUŽLIAK, Peter; Jan NOVÁK a Miroslav NOVÁK

Základní údaje

Originální název

Vascular endothelial growth factor inhibitor-induced hypertension: from pathophysiology to prevention and treatment based on long-acting nitric oxide donors.

Autoři

KRUŽLIAK, Peter (203 Česká republika, garant); Jan NOVÁK (203 Česká republika, domácí) a Miroslav NOVÁK (203 Česká republika)

Vydání

American Journal of Hypertension, Oxford, Oxford University Press, 2014, 0895-7061

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30105 Physiology

Stát vydavatele

Velká Británie a Severní Irsko

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 2.852

Kód RIV

RIV/00216224:14110/14:00075844

Organizační jednotka

Lékařská fakulta

DOI

http://dx.doi.org/10.1093/ajh/hpt201

UT WoS

000328395500002

EID Scopus

2-s2.0-84890455222

Klíčová slova anglicky

NO donors; VEGF.; angiogenesis inhibitors; blood pressure; hypertension; nitric oxide (NO)

Štítky

EL OK

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 13. 1. 2015 15:45, Soňa Böhmová

Anotace

V originále

Hypertension is the most common adverse effect of the inhibitors of vascular endothelial growth factor (VEGF) pathwaybased therapy (VEGF pathway inhibitors therapy, VPI therapy) in cancer patients. VPI includes monoclonal antibodies against VEGF, tyrosine kinase inhibitors, VEGF Traps, and so-called aptamers that may become clinically relevant in the future. All of these substances inhibit the VEGF pathway, which in turn causes a decrease in nitric oxide (NO) and an increase in blood pressure, with the consequent development of hypertension and its final events (e.g., myocardial infarction or stroke). To our knowledge, there is no current study on how to provide an optimal therapy for patients on VPI therapy with hypertension. This review summarizes the roles of VEGF and NO in vessel biology, provides an overview of VPI agents, and suggests a potential treatment procedure for patients with VPI-induced hypertension.

Citovat

KRUŽLIAK, Peter; Jan NOVÁK a Miroslav NOVÁK. Vascular endothelial growth factor inhibitor-induced hypertension: from pathophysiology to prevention and treatment based on long-acting nitric oxide donors. American Journal of Hypertension. Oxford: Oxford University Press, 2014, roč. 27, č. 1, s. 3-13. ISSN 0895-7061. Dostupné z: https://dx.doi.org/10.1093/ajh/hpt201.

@article{1187261,
   author = {Kružliak, Peter and Novák, Jan and Novák, Miroslav},
   article_location = {Oxford},
   article_number = {1},
   doi = {http://dx.doi.org/10.1093/ajh/hpt201},
   keywords = {NO donors; VEGF.; angiogenesis inhibitors; blood pressure; hypertension; nitric oxide (NO)},
   language = {eng},
   issn = {0895-7061},
   journal = {American Journal of Hypertension},
   title = {Vascular endothelial growth factor inhibitor-induced hypertension: from pathophysiology to prevention and treatment based on long-acting nitric oxide donors.},
   volume = {27},
   year = {2014}
}

TY  - JOUR
ID  - 1187261
AU  - Kružliak, Peter - Novák, Jan - Novák, Miroslav
PY  - 2014
TI  - Vascular endothelial growth factor inhibitor-induced hypertension: from pathophysiology to prevention and treatment based on long-acting nitric oxide donors.
JF  - American Journal of Hypertension
VL  - 27
IS  - 1
SP  - 3-13
EP  - 3-13
PB  - Oxford University Press
SN  - 08957061
KW  - NO donors
KW  - VEGF.
KW  - angiogenesis inhibitors
KW  - blood pressure
KW  - hypertension
KW  - nitric oxide (NO)
N2  - Hypertension is the most common adverse effect of the inhibitors of vascular endothelial growth factor (VEGF) pathwaybased therapy (VEGF pathway inhibitors therapy, VPI therapy) in cancer patients. VPI includes monoclonal antibodies against VEGF, tyrosine kinase inhibitors, VEGF Traps, and so-called aptamers that may become clinically relevant in the future. All of these substances inhibit the VEGF pathway, which in turn causes a decrease in nitric oxide (NO) and an increase in blood pressure, with the consequent development of hypertension and its final events (e.g., myocardial infarction or stroke). To our knowledge, there is no current study on how to provide an optimal therapy for patients on VPI therapy with hypertension. This review summarizes the roles of VEGF and NO in vessel biology, provides an overview of VPI agents, and suggests a potential treatment procedure for patients with VPI-induced hypertension.
ER  -

KRUŽLIAK, Peter; Jan NOVÁK a Miroslav NOVÁK. Vascular endothelial growth factor inhibitor-induced hypertension: from pathophysiology to prevention and treatment based on long-acting nitric oxide donors. \textit{American Journal of Hypertension}. Oxford: Oxford University Press, 2014, roč.~27, č.~1, s.~3-13. ISSN~0895-7061. Dostupné z: https://dx.doi.org/10.1093/ajh/hpt201.

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