The Renin-Angiotensin-System (RAS) molecular network has been widely studied, especially with attention to
angiotensin II, the main effector peptide among RAS. The relation of Ang II to hypertension pathogenesis has led to research
being extended to other molecules from the RAS, such as angiotensin III and IV, angiotensin (1-5), and angiotensin
(1-9). Moreover, great pharmacologic advances have been made in hypertension treatment by inhibiting renin and angiotensin
converting enzymes and blocking the bonding of angiotensin II to its receptor AT1. Thus, RAS molecular signaling
and its effect on blood pressure as well as its relationship to renal function and cardiovascular disease are still being investigated.
It is a great challenge to fully cover and understand all molecules from the RAS, especially those that interfere
with or have vasoactive properties. Some of these targets respond to exercise, stimulating nitric oxide synthesis and endothelial
vasodilation. The activation of these specific molecules via exercise is a systematic way of controlling high blood
pressure without pharmacological treatment. Angiotensin (1-7) has been focused due to its vasodilation properties and its
responses to exercise, improving vascular function. Thus, stimulation of the ACE2/Ang (1-7)/Mas axis has been gaining
ground as a prospective clinical means to attenuate cardiovascular diseases such as hypertension by modulating RAS activity.
This review focuses on the vasoactive peptides from the RAS, their responses to exercise and possible trends for
pharmacological development. In several cases where exercise training is not achievable, cardiovascular drug therapy with
vasodilator peptides may possibly be an option.