Assuntos

RESUMO

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

Assuntos

RESUMO

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.

Assuntos

RESUMO

We determined the effects of DuP753 and PD123319 (both nonpeptides and selective antagonists of the AT1 and AT2 angiotensin receptors, respectively), and [Sar(l), Ala(8)]ANG II (a non-selective peptide antagonist of angiotensin receptors)on water and 3 per cent NaCl intake induced by administration of angiotensin II (ANG II) into the paraventricular nucleus (PVN) of sodium-depleted Holtzman rats weighing 250-300 g. Twenty hours before the experiments, the rats were depleted of sodium using furosemide (10 ng/rat, sc). The volume of drug solution injected was 0.5 mul over a period of 10-15 sec. Water and sodium intake were measured at 0.25, 0.5, 1.0 and 2.0 h. Pre-treatment with DuP753 (l4 rats) at a dose of 60 ng completely abolished the water intake induced by injection of 12 ng of ANG II (15 rats) (6.4 ñ 0.6 vs 1.4 ñ 0.3 ml/2 h), whereas [Sar(l), Ala(8)]ANG II (l2 rats) and PDl23319 (10 rats) at the doses of 60 ng partially blocked water intake (6.4 ñ 0.6 vs 2.9 ñ 0.5 and 2.7 ñ 0.2 ml/2 h, respectively). In the same animals, [Sar(l), Ala(8)]ANG II, DuP753, and PDl23319 blocked the sodium intake induced by ANG II (9.2 ñ 1.6 vs 3.3 ñ 0.6, 1.8 ñ 0.3, and 1.4 ñ 0.2 ml/2 h, respectively). These results indicate that both DuP753 and PD123319, administered into the PVN, blocked the water and sodium intake induced by administration of ANG II into the same site.

Assuntos

RESUMO

We tested the effects of estradiol, progesterone and testosterone on water and salt intake induced by angiotensin II (ANG II) injected into the third ventricle of female Holtzman rats weighing 250-300 g. The water and salt ingestion observed after 120 min in the control experiments (injection of 0.5µl of 0.15 M NaCl into the third ventricle) was 1.6 ñ 0.3 ml (N = 10) and 0,3 ñ 0.1 ml (N = 8) in intact rats, respectively, and 1.4 ñ 0.3 ml (N = 10) and 0.2 ñ 0.1 (N = 8) in ovariectomized rats, respectively. ANG II injected in intact rats (4, 6, 12, 25, and 50 ng, icv, in 0,5 µl saline) induced an increase in water intake (4.3 ñ 0.6, 5.4 ñ 0.7, 7.8 ñ 0.8, 10.4 ñ 1.2, 11.2 ñ 1.4 ml/120 min, respectively) ( N = 43). The same doses of icv ANG II in intact increased the 3 per cent NaCl intake (0.9 ñ 0,2, 1.4 ñ 0,3, 2,3 ñ 0.4, 2,2 ñ 0,3, and 2.5 ñ 0.4 ml/120 min, respectively) (N = 42). When administered to ovariectomized rats ANG II induced comparable amounts of water intake (4.0 ñ 0.5, 4.8 ñ 0.6 ñ 0.7, 9.6 ñ 0.8, and 10.9 ñ 1.2 ml/120 min, respectively (

Assuntos