PubMed · 14630454
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M G Gama, G Rocha. 2003-11-15. The CHARM programme.. https://doi.org/10.1016/s0140-6736(03)14809-x
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AT(1) receptor antagonists may interfere with the haemodynamic determinants of arterial pressure either directly or indirectly through the stimulation of AT(2) receptor provided Ang II is available to interact with them. In order to evaluate the counteracting haemodynamic effect of AT(2) receptor, a prospective, randomized, controlled experimental study was carried out in anaesthetised juvenile pigs. Pigs were randomly assigned to receive placebo (n = 6), valsartan, an AT(1) receptor antagonist (a-AT(1) group; n = 6), or valsartan and PD 123319, an AT(2) receptor antagonist (a-AT(1-2) group; n = 6) after anaesthesia and before hypovolaemia by 20% of the total estimated blood volume. Thirty minutes after bleeding, the mean arterial pressure decreased significantly and similarly in the three groups (25-30%). The placebo group had a significant decrease in cardiac output (CO) without significant change in systemic vascular resistance (SVR). Conversely, in the a-AT(1) group, SVR decreased significantly with a moderate change in CO and addition of the AT(2) antagonist to the AT(1) antagonist (a-AT(1-2) group) did not abolish the lowering in SVR. The results suggest that AT(2) receptor has only a small if any contribution in the vasodilatation observed in the AT(1)-blockade group.
It has been shown that central or peripheral injections of the peptide relaxin induces water intake, not sodium intake in rats. Important inhibitory mechanisms involving serotonin and other neurotransmitters in the control of water and NaCl intake have been demonstrated in the lateral parabrachial nucleus (LPBN). In the present study, we investigated the effects of bilateral injections of methysergide (serotonergic receptor antagonist) into the LPBN on intracerebroventricular (i.c.v.) relaxin-induced water and NaCl intake in rats. Additionally, the effect of the blockade of central angiotensin AT(1) receptors with i.c.v. losartan on relaxin-induced water and NaCl intake in rats treated with methysergide into the LPBN was also investigated. Male Holtzman rats with cannulas implanted into the lateral ventricle (LV) and bilaterally in the LPBN were used. Intracerebroventricular injections of relaxin (500 ng/1 microl) induced water intake (5.1+/-0.7 ml/120 min), but not significant 1.8% NaCl intake (0.5+/-0.4 ml/120 min). Bilateral injections of methysergide (4 microg/0.2 microl) into the LPBN strongly stimulated relaxin-induced 1.8% NaCl intake (34.5+/-10.9 ml/120 min) and slightly increased water intake (10.5+/-4.9 ml/120 min). The pretreatment with i.c.v. losartan (100 microg/1 microl) abolished the effects of i.c.v. relaxin combined with LPBN methysergide on 1.8% NaCl intake (0.5+/-0.4 ml/120 min). Losartan (100 microg/1 microl) also abolished relaxin-induced water intake in rats injected with methysergide into the LPBN (1.6+/-0.8 ml/120 min) or not (0.5+/-0.3 ml/120 min). Losartan (50 microg/1 microl) partially reduced the effects of relaxin. The results show that central relaxin interacting with central angiotensinergic mechanisms induces NaCl intake after the blockade of LPBN serotonergic mechanisms.