Effect of acute volume expansion associated with salt load on the profile of plasma angiotensins in rats.

We measured the changes produced in renin and the peptide components of the circulating renin-angiotensin system by acute volume expansion alone or associated with salt load in rats. With both maneuvers, there was a decrease of plasma renin activity (PRA) and plasma angiotensin (Ang) concentrations, but the changes were more pronounced in the salt-load group. In contrasting to Ang I and Ang II, plasma Ang-(1-7) concentration decreased significantly only within 60 min of 5.0% NaCl infusion (19.5 +/- 2.9 vs 30.5 +/- 1.9 pg/ml in the control group). As expected, plasma vasopressin increased markedly in the animals submitted to acute salt load (144.0 +/- 42.0 vs 5.0 +/- 0.2 pg/ml in the control group). The dissociation between the changes in plasma Ang-(1-7) and that of other plasma angiotensins is consistent with our previous studies using chronic salt load, and suggests that during acute volume expansion associated with salt load Ang I is preferentially converted to Ang-(1-7). In contrast to vasopressin, however, plasma Ang-(1-7) concentration increased only after chronic salt load, suggesting that this angiotensin may be more involved with long-term mechanisms of control of hydromineral balance.

Plasma angiotensin(1-7) immunoreactivity is increased by salt load, water deprivation, and hemorrhage.

In this study we investigated the effects of dehydration and hemorrhage on circulating levels of the heptapeptide, angiotensin(1-7). In water-deprived rats, a twofold increase in plasma angiotensin(1-7) was associated with similar increases in plasma renin activity, and angiotensin I and angiotensin II levels. In salt-loaded rats, plasma angiotensin(1-7) levels increased fourfold; however, other components of the renin-angiotensin system were suppressed or unchanged. In salt-loaded rats, increases in plasma angiotensin II levels in response to hemorrhage in normal rats were severely blunted, whereas angiotensin(1-7) plasma levels increased proportionately to the loss of blood volume. These results suggest that angiotensin(1-7) plasma concentration can be selectively regulated during dehydration and hemorrhage.