Detailed Information on Publication Record

KRUŽLIAK, Peter, Jan NOVÁK and 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, vol. 27, No 1, p. 3-13. ISSN 0895-7061. Available from: https://dx.doi.org/10.1093/ajh/hpt201.

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Basic information
Original name	Vascular endothelial growth factor inhibitor-induced hypertension: from pathophysiology to prevention and treatment based on long-acting nitric oxide donors.
Authors	KRUŽLIAK, Peter (203 Czech Republic, guarantor), Jan NOVÁK (203 Czech Republic, belonging to the institution) and Miroslav NOVÁK (203 Czech Republic).
Edition	American Journal of Hypertension, Oxford, Oxford University Press, 2014, 0895-7061.

Other information
Original language	English
Type of outcome	Article in a journal
Field of Study	30105 Physiology
Country of publisher	United Kingdom of Great Britain and Northern Ireland
Confidentiality degree	is not subject to a state or trade secret
Impact factor	Impact factor: 2.852
RIV identification code	RIV/00216224:14110/14:00075844
Organization unit	Faculty of Medicine
Doi	http://dx.doi.org/10.1093/ajh/hpt201
UT WoS	000328395500002
Keywords in English	NO donors; VEGF.; angiogenesis inhibitors; blood pressure; hypertension; nitric oxide (NO)
Tags	EL OK
Tags	International impact, Reviewed
Changed by	Changed by: Soňa Böhmová, učo 232884. Changed: 13/1/2015 15:45.

Abstract
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.

Abstract

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.