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.