the physiological aspects involving host components in
this process are still poorly understood. Our results provide the
first evidence of the important role of RAS components in
erythrocyte infection by P. falciparum. Here we show that Ang II,
through its carboxypeptidase-mediated metabolic product, Ang-
(1–7), decreases infection of new erythrocytes during development
of the P. falciparum blood stage. This effect of Ang-(1–7) is specific
and probably involves a MAS-mediated PKA inhibition.
The first question that arises from our results is: What is the
source of Ang II involved in the modulation of the erythrocyte
cycle of P. falciparum? Recently, local tissue generation of Ang II
has been described; this peptide could have paracrine or autocrine
effects [21–24]. Therefore, it is possible to postulate that Ang II
produced locally by different tissues such as immune and vascular
cells could modulate the erythrocyte cycle of P. falciparum.