Development of angiotensin (1-7) as an agent to accelerate dermas repair

Angiotensin II has been shown to be a potent agent in the acceleration of w ound repair. Angiotensin (1-7), a fragment of angiotensin II that is not hy pertensive, was found to be comparable to angiotensin II in accelerating de rmal healing. This activity was evaluated in four models: rat and diabetic mouse full-thickness excisional wounds, rat random flap; and guinea pig par tial thickness thermal injury. In all models, angiotensin (1-7) was compara ble to angiotensin ii. Angiotensin (1-7) accelerated the closure of wounds in diabetic mice and rats, In diabetic mice the resultant tissue at day 25 after injury was more comparable to normal tissue than the fibrotic scar ob served in placebo-treated wounds. In the random flap modes, angiotensin (1- 7) was comparable to angiotensin II in maintaining flap viability (approxim ately 82%) and flap survival (40%). Finally, angiotensin (1-7) increased pr oliferation in the hair follicles at the edge of the wound and site of ther mal injury; and the number of patent blood vessels on day 7 after partial t hickness thermal injury. These data may be partially explained by the effec t of angiotensin II and angiotensin (1-7) on keratinocyte proliferation. Wh ite platelet-derived growth factor had no effect on keratinocyte proliferat ion, angiotensin II and angiotensin (1-7) significantly increased keratinoc yte proliferation. These data show that angiotensin(1-7) is comparable to a ngiotensin II in accelerating skin repair. Furthermore, the hypertensive an d wound healing effects can be separated within the family of angiotensin p eptides.