Across the entire cohort, the delivered dose of exogenous angiotensin II would overcome any inherent angiotensin-converting enzyme defects, so it is likely that attenuation of the MAP response to angiotensin II in the > 5 ng kg−1 min−1 subgroup may be influenced by other factors, including down-regulation of angiotensin I/II receptors in conditions such as sepsis and/or biofeedback to the production of vasodilatory peptides [20–22]. This evidence concerns the gene AGT and Sepsis.