Saad W A, Camargo L A, Silveira J E, Saad R, Camargo G M
Department of Physiology, School of Dentistry, Paulista State University, UNESP, Brazil.
J Physiol Paris. 1998 Feb;92(1):25-30. doi: 10.1016/s0928-4257(98)80019-3.
In the present experiments we investigated a possible involvement of imidazoline receptors of the paraventricular nucleus (PVN) of the hypothalamus on the pressor effects of the angiotensin II (ANG II) injected into the subfornical organ (SFO), in male Holtzman rats (250-300 g) with a cannula implanted into the third ventricle (3rdV), PVN and SFO. At first we tested the participation of alpha 2 and imidazoline agonist and antagonist compounds on the pressor effect of ANG II injected into the 3rdV. Based on the results we may conclude that clonidine associated with rilmenidine was able to block the hypertensive response to ANG II. The ANG II (20 pmol) injected into SFO induced a robust increase in blood pressure (37 +/- 2 mmHg). Isotonic saline (0.15 M) NaCl did not produce any change in blood pressure (5 +/- 2 mmHg). The injection of rilmenidine (30 micrograms/kg/1 microL), an imidazoline agonist agent injected into PVN before ANG II injection into SFO, blocked the pressor effect of ANG II (5 +/- 2 mmHg). Also, the injection of idazoxan (60 micrograms/kg/microL) before rilmenidine blocked the inhibitory effect of rilmenidine on blood pressure (39 +/- 4 mmHg). The injection of clonidine (20 nmol/microL) prior to ANG II into the 3rdV produced a decreased in arterial blood pressure (37 +/- 2 mmHg) to (15 +/- 4 mmHg). The injection of yohimbine (80 nmol/microL) prior to clonidine blocked the effect of clonidine on the effect of ANG II (27 +/- 2 mmHg). The injection of rilmenidine prior to ANG II also induced a decrease in arterial blood pressure (10 +/- 3 mmHg). The injection of idazoxan prior to rilmenidine also blocked the inhibitory effect of rilmenidine (24 +/- 3 mmHg). In summary, the present study demonstrated that rilmenidine decreases the hypertensive effect of ANG II, with more potency than clonidine, even when injected into 3rdV or PVN. This study established that the PVN interacts with SFO by imidazoline receptors in order to control the arterial blood pressure.
在本实验中，我们研究了下丘脑室旁核（PVN）的咪唑啉受体是否可能参与注入穹窿下器官（SFO）的血管紧张素II（ANG II）的升压作用，实验对象为雄性霍尔兹曼大鼠（250 - 300克），这些大鼠已植入第三脑室（3rdV）、PVN和SFO的插管。首先，我们测试了α2和咪唑啉激动剂及拮抗剂化合物对注入3rdV的ANG II升压作用的参与情况。根据结果我们可以得出结论，可乐定与利美尼定联合能够阻断对ANG II的高血压反应。注入SFO的ANG II（20皮摩尔）可使血压显著升高（37±2毫米汞柱）。等渗盐水（0.15 M）NaCl对血压无任何影响（5±2毫米汞柱）。在向SFO注入ANG II之前，向PVN注入咪唑啉激动剂利美尼定（30微克/千克/1微升）可阻断ANG II的升压作用（5±2毫米汞柱）。此外，在注入利美尼定之前注入伊达唑胺（60微克/千克/微升）可阻断利美尼定对血压的抑制作用（39±4毫米汞柱）。在向3rdV注入ANG II之前注入可乐定（20纳摩尔/微升）可使动脉血压从（37±2毫米汞柱）降至（15±4毫米汞柱）。在注入可乐定之前注入育亨宾（80纳摩尔/微升）可阻断可乐定对ANG II作用的影响（27±2毫米汞柱）。在注入ANG II之前注入利美尼定也可使动脉血压降低（10±3毫米汞柱）。在注入利美尼定之前注入伊达唑胺也可阻断利美尼定的抑制作用（24±3毫米汞柱）。总之，本研究表明，利美尼定可降低ANG II引起的高血压作用，其效力比可乐定更强，即使注入3rdV或PVN时也是如此。本研究证实，PVN通过咪唑啉受体与SFO相互作用以控制动脉血压。
