Nicotine stimulates angiogenesis and promotes tumor growth and atherosclerosis.
We provide anatomic and functional evidence that nicotine induces angiogenesis. We also show that nicotine accelerates the growth of tumor and atheroma in association with increased neovascularization. Nicotine increased endothelial-cell growth and tube formation in vitro, and accelerated fibrovascular growth in vivo. In a mouse model of hind-limb ischemia, nicotine increased capillary and collateral growth, and enhanced tissue perfusion. In mouse models of lung cancer and atherosclerosis, we found that nicotine enhanced lesion growth in association with an increase in lesion vascularity. These effects of nicotine were mediated through nicotinic acetylcholine receptors at nicotine concentrations that are pathophysiologically relevant. The endothelial production of nitric oxide, prostacyclin and vascular endothelial growth factor might have a role in these effects.
Heeschen
C
C
Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California, USA.
Jang
J J
JJ
Weis
M
M
Pathak
A
A
Kaji
S
S
Hu
R S
RS
Tsao
P S
PS
Johnson
F L
FL
Cooke
J P
JP
D000818:Animals; D001161:Arteriosclerosis / Q000150:complications* / Q000473:pathology; D018827:Carcinoma, Lewis Lung / Q000098:blood supply* / Q000473:pathology*; D008175:Lung Neoplasms / Q000098:blood supply* / Q000473:pathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009389:Neovascularization, Pathologic / Q000209:etiology*; D009538:Nicotine / Q000494:pharmacology*
D009538:Nicotine