Angiogenesis and arteriogenesis are increased in fibrin gel chambers implanted in prehypertensive spontaneously hypertensive rats.
OBJECTIVE
Microvascular rarefaction by an unbalanced angiogenesis could promote the onset of hypertension in spontaneously hypertensive rats and in hypertensive patients. We studied the angiogenic potency in the fibrin gel chamber model in prehypertensive spontaneously hypertensive rats and their controls, Wistar-Kyoto rats.


METHODS
Four-week-old prehypertensive spontaneously hypertensive rats (n = 9) and Wistar-Kyoto rats (n = 9) were implanted with four fibrin gel chambers located in the dorsal subcutaneous space. After 14 days, vasculoconjunctive buds had invaded the fibrin gel through the 10 hole-perforated bottom slip of the chamber. The intact vascular buds were studied using optical microscopy, alpha-actin and von Willebrand factor stainings. Capillaries and arterialized vessels were counted in three peripheral and one central field in each bud. The immunodetection of vascular endothelial growth factor and fibroblast growth factor 2 was performed on the neovascular buds.


RESULTS
In fibrin chambers implanted in spontaneously hypertensive rats, the number of peripheral vessels was significantly higher than in Wistar-Kyoto rats. There were significantly more arterialized vessels in spontaneously hypertensive rats compared with Wistar-Kyoto rats. The number of immunostained cells for fibroblast growth factor 2 was significantly greater in spontaneously hypertensive rats compared with Wistar-Kyoto rats. There was no significant difference in vascular endothelial growth factor staining between the two strains of rats.


CONCLUSIONS
Angiogenesis and arteriogenesis are increased in fibrin chambers implanted in prehypertensive spontaneously hypertensive rats compared with Wistar-Kyoto rats. These results argue against microvascular rarefaction as a cause of hypertension using this model of angiogenesis.
Laboratoire de Recherche sur l'Angiogenèse, Faculté de Médecine, Université Louis Pasteur, 11 rue Humann, 67085 Strasbourg, France.
Philippe
P
Hudlett
Agnès
A
Neuville
Anne
A
Miternique
Christophe
C
Griffon
Denis
D
Weltin
Dominique
D
Stephan
D000199:Actins / Q000378:metabolism; D000818:Animals; D001158:Arteries / Q000254:growth & development*; D004343:Drug Implants / Q000378:metabolism*; D005337:Fibrin / Q000378:metabolism* / Q000494:pharmacology; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism; D005782:Gels; D006973:Hypertension / Q000503:physiopathology*; D007150:Immunohistochemistry; D008954:Models, Biological; D018919:Neovascularization, Physiologic / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D014841:von Willebrand Factor / Q000378:metabolism
D000199:Actins; D004343:Drug Implants; D005782:Gels; D042461:Vascular Endothelial Growth Factor A; D014841:von Willebrand Factor; D016222:Fibroblast Growth Factor 2; D005337:Fibrin