| First Author | Oliverio MI | Year | 2000 |
| Journal | Hypertension | Volume | 35 |
| Issue | 2 | Pages | 550-4 |
| PubMed ID | 10679496 | Mgi Jnum | J:103283 |
| Mgi Id | MGI:3609082 | Doi | 10.1161/01.hyp.35.2.550 |
| Citation | Oliverio MI, et al. (2000) Regulation of sodium balance and blood pressure by the AT(1A) receptor for angiotensin II. Hypertension 35(2):550-4 |
| abstractText | To examine the role of the angiotensin II (AT)(1A) receptor in the regulation of blood pressure and sodium balance, we measured systolic blood pressure responses in AT(1A) receptor-deficient (Agtr1a-/-) and wild-type (Agtr1a+/+) mice while dietary sodium content was systematically altered. On a 0.4% sodium diet, systolic blood pressures were significantly lower in Agtr1a-/- than in +/+ mice. In Agtr1a+/+ mice, changing dietary sodium content did not affect blood pressure. In contrast, when Agtr1a-/- mice were fed a high-salt diet (6% NaCl), their systolic blood pressures increased significantly from 79+/-4 to 94+/-4 mm Hg (P<0.006). The low blood pressures of Agtr1a-/- mice decreased further while on a low-salt diet from 82+/-3 to 69+/-3 mm Hg (P<0.03). On the high-salt diet, urinary sodium excretion increased to similar levels in Agtr1a+/+ and -/- mice. Although urinary sodium excretion was substantially reduced in both groups during the low-salt diet, cumulative sodium balances became negative in Agtr1a-/- mice despite a 6-fold increase in urinary aldosterone. We infer, therefore, that the reduced blood pressures in Agtr1a-/- mice on a normal diet are caused by depletion of sodium and extracellular volume. Their 'sodium sensitivity' suggests a critical role for renal AT(1A) receptors to modulate sodium handling. |
