The present studies were performed to quantify circulating components of the renin-angiotensin-aldosterone axis and to determine the functional importance of this system during alterations in sodium intake in conscious mice. Increasing sodium intake from ∼200 to 1,000 μeq/day significantly decreased plasma renin concentration from 472 ± 96 to 304 ± 83 ng ANG I·ml-1·h-1 (n = 5) but did not alter plasma renin activity from the low-sodium level of 7.7 ± 1.1 ng ANG I·ml-1·h-1. Despite the elevated plasma renin concentration, plasma ANG II in mice on low-sodium level averaged 14 ± 3 pg/ml and was significantly suppressed to 6 ± 1 pg/ml by high-sodium intake (n = 7). Consistent with the modulation of ANG II, plasma aldosterone significantly decreased from 41 ± 8 to 8 ± 3 ng/dl when sodium intake was elevated (n = 6). In a final set of experiments, the continuous infusion of ANG II (20 ng·kg-1·min-1) led to a mild salt-sensitive increase in mean arterial pressure from 108 ± 2 to 131 ± 2 mmHg as sodium intake was varied from low to high (n = 7). In vehicle-infused mice, mean arterial pressure was unaltered from 109 ± 2 mmHg when sodium intake was increased (n = 6). These studies indicate that the physiological suppression of circulating ANG II may be required to maintain a constancy of arterial pressure during alterations in sodium intake in normal mice.
|Original language||English (US)|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|Issue number||3 50-3|
|State||Published - 2001|
- Blood pressure
ASJC Scopus subject areas
- Physiology (medical)