Role of angiotensin II and vasopressin receptors within the supraoptic nucleus in water and sodium intake induced by the injection of angiotensin II into the medial septal area

In this study we investigated the effects of the injection into the supraoptic nucleus (SON) of non-peptide AT1- and AT2-angiotensin II (ANG II) receptor antagonists, DuP753 and PD123319, as well as of the arginine-vasopressin (AVP) receptor antagonist d(CH2)5-Tyr(Me)-AVP, on water and 3 percent NaCl intake induced by the injection of ANG II into the medial septal area (MSA). The effects on water or 3 percent NaCl intake were assessed in 30-h water-deprived or in 20-h water-deprived furosemide-treated adult male rats, respectively. The drugs were injected in 0.5 µl over 30-60 s. Controls were injected with a similar volume of 0.15 M NaCl. Antagonists were injected at doses of 20, 80 and 180 nmol. Water and sodium intake was measured over a 2-h period. Previous administration of the AT1 receptor antagonist DuP753 into the SON decreased water (65 percent, N = 10, P<0.01) and sodium intake (81 percent, N = 8, P<0.01) induced by the injection of ANG II (10 nmol) into the MSA. Neither of these responses was significantly changed by injection of the AT2-receptor antagonist PD123319 into the SON. On the other hand, while there was a decrease in water intake (45 percent, N = 9, P<0.01), ANG II-induced sodium intake was significantly increased (70 percent, N = 8, P<0.01) following injection of the V1-type vasopressin antagonist d(CH2)5-Tyr(Me)-AVP into the SON. These results suggest that both AT1 and V1 receptors within the SON may be involved in water and sodium intake induced by the activation of ANG II receptors within the MSA. Furthermore, they do not support the involvement of MSA AT2 receptors in the mediation of these responses

Central interaction between atrial natriuretic peptide and angiotensin II in the control of sodium intake and excretion in female rats

We investigated the effects of estrogen on sodium intake and excretion induced by angiotestin II (ANG II), atrial natriuretic peptide (ANP) or ANG II plus ANP injected into median preoptic nucleus MnPO). Female Holtzman rats weighing 250-300 g were used. Sodium ingestion and excretion 120 min after the injection of 0.5 mul of 0.15 M NaCl into the MnPO were 0.3 + 7 muEq in intact rats, 0.5 + 0.2 ml (N = 10) and 27 + 6 muEq in ovariectmized rats, and 0.2 + 0.08 (N = 11) and 36 + 8 muEq in estrogen-treated ovariectomized (50 mug/day for 21 days) rats, respectively. ANG II (21 muM) injection in intact, ovariectomized, and estrogen-treated ovariectomized rats increased sodium intake (3.8 + 0.4, 1.8 + 0.3 and 1.2 + 0.2 ml/120 min, respectively) (N = 11) and increased sodium excretion (166 + 18,82 + 22 and 86 + 22 and 86 + 12 muEq/120 min, respectively (N = 11). ANP (65 muM) injection in intact (N = 11), ovariectomized (N = 10) and estrogen-treated ovariectomized (N = 10) rats increased sodium intake (1.4 + 0.2, 1.8 + 0.3, and 1.7 + 0.3 ml/120 min, respectively) and sodium excretion (178 + 19, 187 + 9, and 232 + 29 muEq/120 min, respectively). Concomitant injection of ANG II and ANP into the MnPO of intact (N = 12), ovariectomized (N = 10) and estrogentreated ovariectomized (N = 10) rats caused smaller effects than those produced by each peptide given alone: 1.3 + 0.2, 0.9 + 0.2 and 0.3 + 0.1 ml/120 min for sodium intake, respectively, and 86 + 9,58 + 7, and 22 + 4 muEq/120 min for sodium excretion, respectively. Taken together, these results demonstrate that there is an antagonistic interaction of ANP and ANG II on sodium intake and excretion, and that reproductive hormones affect this interaction.