Why the study?
Does inhibition of angiotensin II or VEGF prevent angiogenesis induced by short-term exercise training in male Sprague-Dawley rats?
Does inhibition of angiotensin II or VEGF prevent angiogenesis induced by short-term exercise training in male Sprague-Dawley rats?
Angiotensin II and VEGF are essential mediators of skeletal muscle angiogenesis induced by short-term exercise training.
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Should not alter exercise advice for patients on ACEi/ARBs; leaves open translation to human cardiac or skeletal muscle angiogenesis.
Results from our laboratory have suggested a pathway involving angiotensin II type 1 (AT(1)) receptors and vascular endothelial growth factor (VEGF) in angiogenesis induced by electrical stimulation. The present study investigated if similar mechanisms underlie the angiogenesis induced by short-term exercise training. Seven days before training and throughout the training period, male Sprague-Dawley rats received either captopril or losartan in their drinking water. Rats underwent a 3-day treadmill training protocol. The tibialis anterior and gastrocnemius muscles were harvested under anesthesia and lightly fixed in formalin (vessel density) or frozen in liquid nitrogen (VEGF expression). In controls, treadmill training resulted in a significant increase in vessel density in all muscles studied. However, the angiogenesis induced by exercise was completely blocked by either losartan or captopril. Western blot analysis showed that VEGF expression was increased in the exercised control group, and both losartan and captopril blocked this increase. The role of VEGF was directly confirmed using a VEGF-neutralizing antibody. These results confirm the role of angiotensin II and VEGF in angiogenesis induced by exercise.
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Amaral et al. (2001) studied this question.
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