Abstract
Essential hypertension may be a consequence of structural and functional alterations of the microvascular network growth resulting partly from abnormal regulation of vascular endothelial growth factor (VEGF), one of the most potent known angiogenic factors. As data from clinical trials on anti-VEGF drugs are becoming available, it is increasingly recognized that VEGF, in addition to being a proliferation and migration factor, is also a maintenance and protection factor for endothelial cells, whose altered regulation may cause a disturbance of vascular homeostasis. Elevated VEGF levels in hypertensive patients were shown to correlate with cardiovascular risk, early microvascular and target organ damage; accordingly treatment of hypertension significantly reduced VEGF levels. Recently and in agreement with the theory that impaired angiogenesis can contribute to increased peripheral resistance and raised blood pressure (BP), an involvement of VEGF gene promoter polymorphisms in the pathophysiology of hypertension has been hypothesized. In the last decade, anti-VEGF drugs have been used in clinical practice, especially in the oncology field. This review will summarize the present understanding of the contribution of VEGF to neoangiogenesis in hypertension and its possible role as a marker of vascular damage. Given the well established effects that antihypertensive drugs exert on the vasculature beyond BP lowering (pleiotropic effects), we will also discuss the effects of antihypertensive treatment on circulating VEGF levels. The biological mechanism and clinical impact of hypertensive complications during anti-angiogenic treatments will also be reviewed.
| Original language | English |
|---|---|
| Pages (from-to) | 479-493 |
| Number of pages | 15 |
| Journal | Current Vascular Pharmacology |
| Volume | 10 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - Jul 2012 |
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Keywords
- Angiogenesis
- Antihypertensive drugs
- Bevacizumab
- Endothelium
- Essential hypertension
- Vascular endothelial growth factor
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Pharmacology
Cite this
Angiogenesis and hypertension : The dual role of anti-hypertensive and anti-angiogenic therapies. / Ferroni, Patrizia; Della-Morte, David; Palmirotta, Raffaele; Rundek, Tatjana; Guadagni, Fiorella; Roselli, Mario.
In: Current Vascular Pharmacology, Vol. 10, No. 4, 07.2012, p. 479-493.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Angiogenesis and hypertension
T2 - The dual role of anti-hypertensive and anti-angiogenic therapies
AU - Ferroni, Patrizia
AU - Della-Morte, David
AU - Palmirotta, Raffaele
AU - Rundek, Tatjana
AU - Guadagni, Fiorella
AU - Roselli, Mario
PY - 2012/7
Y1 - 2012/7
N2 - Essential hypertension may be a consequence of structural and functional alterations of the microvascular network growth resulting partly from abnormal regulation of vascular endothelial growth factor (VEGF), one of the most potent known angiogenic factors. As data from clinical trials on anti-VEGF drugs are becoming available, it is increasingly recognized that VEGF, in addition to being a proliferation and migration factor, is also a maintenance and protection factor for endothelial cells, whose altered regulation may cause a disturbance of vascular homeostasis. Elevated VEGF levels in hypertensive patients were shown to correlate with cardiovascular risk, early microvascular and target organ damage; accordingly treatment of hypertension significantly reduced VEGF levels. Recently and in agreement with the theory that impaired angiogenesis can contribute to increased peripheral resistance and raised blood pressure (BP), an involvement of VEGF gene promoter polymorphisms in the pathophysiology of hypertension has been hypothesized. In the last decade, anti-VEGF drugs have been used in clinical practice, especially in the oncology field. This review will summarize the present understanding of the contribution of VEGF to neoangiogenesis in hypertension and its possible role as a marker of vascular damage. Given the well established effects that antihypertensive drugs exert on the vasculature beyond BP lowering (pleiotropic effects), we will also discuss the effects of antihypertensive treatment on circulating VEGF levels. The biological mechanism and clinical impact of hypertensive complications during anti-angiogenic treatments will also be reviewed.
AB - Essential hypertension may be a consequence of structural and functional alterations of the microvascular network growth resulting partly from abnormal regulation of vascular endothelial growth factor (VEGF), one of the most potent known angiogenic factors. As data from clinical trials on anti-VEGF drugs are becoming available, it is increasingly recognized that VEGF, in addition to being a proliferation and migration factor, is also a maintenance and protection factor for endothelial cells, whose altered regulation may cause a disturbance of vascular homeostasis. Elevated VEGF levels in hypertensive patients were shown to correlate with cardiovascular risk, early microvascular and target organ damage; accordingly treatment of hypertension significantly reduced VEGF levels. Recently and in agreement with the theory that impaired angiogenesis can contribute to increased peripheral resistance and raised blood pressure (BP), an involvement of VEGF gene promoter polymorphisms in the pathophysiology of hypertension has been hypothesized. In the last decade, anti-VEGF drugs have been used in clinical practice, especially in the oncology field. This review will summarize the present understanding of the contribution of VEGF to neoangiogenesis in hypertension and its possible role as a marker of vascular damage. Given the well established effects that antihypertensive drugs exert on the vasculature beyond BP lowering (pleiotropic effects), we will also discuss the effects of antihypertensive treatment on circulating VEGF levels. The biological mechanism and clinical impact of hypertensive complications during anti-angiogenic treatments will also be reviewed.
KW - Angiogenesis
KW - Antihypertensive drugs
KW - Bevacizumab
KW - Endothelium
KW - Essential hypertension
KW - Vascular endothelial growth factor
UR - http://www.scopus.com/inward/record.url?scp=84861662862&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84861662862&partnerID=8YFLogxK
U2 - 10.2174/157016112800812836
DO - 10.2174/157016112800812836
M3 - Article
C2 - 22272903
AN - SCOPUS:84861662862
VL - 10
SP - 479
EP - 493
JO - Current Vascular Pharmacology
JF - Current Vascular Pharmacology
SN - 1570-1611
IS - 4
ER -