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. CONCLUSION: 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.
OBJECTIVE: Microvascular rarefaction by an unbalanced angiogenesis could promote the onset of hypertension in spontaneously hypertensiverats and in hypertensivepatients. We studied the angiogenic potency in the fibrin gel chamber model in prehypertensive spontaneously hypertensiverats and their controls, Wistar-Kyoto rats. METHODS: Four-week-old prehypertensive spontaneously hypertensiverats (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 hypertensiverats, the number of peripheral vessels was significantly higher than in Wistar-Kyoto rats. There were significantly more arterialized vessels in spontaneously hypertensiverats compared with Wistar-Kyoto rats. The number of immunostained cells for fibroblast growth factor 2 was significantly greater in spontaneously hypertensiverats compared with Wistar-Kyoto rats. There was no significant difference in vascular endothelial growth factor staining between the two strains of rats. CONCLUSION: Angiogenesis and arteriogenesis are increased in fibrin chambers implanted in prehypertensive spontaneously hypertensiverats compared with Wistar-Kyoto rats. These results argue against microvascular rarefaction as a cause of hypertension using this model of angiogenesis.
Authors: A Arkudas; J Tjiawi; A Saumweber; J P Beier; E Polykandriotis; O Bleiziffer; R E Horch; U Kneser Journal: J Cell Mol Med Date: 2008-06-28 Impact factor: 5.310
Authors: Andrea Hartner; Lisa Jagusch; Nada Cordasic; Kerstin Amann; Roland Veelken; Johannes Jacobi; Karl F Hilgers Journal: Front Physiol Date: 2016-08-30 Impact factor: 4.566