简介:内侧视前区(mPOA)参与体温调节控制和血压调制,如通过电刺激该区域或注射氯化钴的研究所示,一种非选择性突触抑制剂.这项研究旨在研究血管紧张素II(AngII)和GABA是否可以在mPOA中起作用以介导心血管和排尿控制途径。方法:在实验前7天,将雌性Wistar大鼠进行立体定向手术以将引导套管植入mPOA中。之后,对动物进行异氟烷麻醉,并接受股动脉和静脉的导管插入术以及膀胱插管术的平均动脉压(MAP),心率(HR),和膀胱内压(IP)记录,分别。在基线MAP之后,HR,和IP录音15分钟,AngII(0.1nM,1μL),氯沙坦(AT-1受体拮抗剂,100nM,1μL),GABA(50mM,将1μL)或盐水(1μL)注射到mPOA中,和变量测量额外的30分钟。在一组不同的老鼠中,AT-1受体,血管紧张素II转换酶(ACE),通过qPCR评估mPOA样品中的GABAa受体基因表达。数据为平均值±SEM,并提交单因素方差分析(Tukey后验)或配对的Studentt-test(P<0.05)。结果:向mPOA中注射AngII可引起明显的低血压(-37±10mmHg,n=6,p=0.024)和心动过缓(-47±20bpm,p=0.030)与盐水(+1±1mmHg和+6±2bpm,n=6)。在将AngII注射到mPOA中后观察到IP的显着增加(72.25±17.91%,p=0.015vs.-1.80±2.98%,n=6,盐水)。在MAP中没有观察到显著的变化,与盐水注射相比,氯沙坦在mPOA中注射后的HR和IP。向mPOA中注射GABA引起MAP和HR的显着下降(-68±2mmHg,n=6,p<0.0001和-115±14bpm,n=6,p=0.0002vs.-1±1mmHg和+4±2bpm,n=6,盐水),但未观察到IP的显著变化。AT-1受体,在所有mPOA样品中观察到ACE和GABAa受体mRNA表达。讨论:因此,在雌性老鼠中,在mPOA中AngII介导的传递涉及心血管调节和中枢排尿途径的控制。依赖于mPOA中AT-1受体的阶段性控制似乎参与了这些心血管和膀胱内3参数的调节。相比之下,mPOA中的GABA能传递参与麻醉雌性大鼠的心血管控制途径,然而,这种神经传递不参与排尿控制。
Introduction: The medial preoptic area (mPOA) participates in thermoregulatory control and blood pressure modulation as shown by studies with electrical stimulation of this area or cobalt chloride injection, a non-selective synapse inhibitor. This study aimed to investigate whether angiotensin II (Ang II) and GABA could act or not in the mPOA to mediate the cardiovascular and
micturition control pathways. Methods: Female Wistar rats were submitted to stereotaxic surgery for implantation of a guide cannula into the mPOA 7 days prior to the experiments. Afterwards, the animals were isoflurane- anesthetized and submitted to the catheterization of the femoral artery and vein and urinary bladder cannulation for mean arterial pressure (MAP), heart rate (HR), and intravesical pressure (IP) recordings, respectively. After the baseline MAP, HR, and IP recordings for 15 min, Ang II (0.1 nM, 1 μL), losartan (AT-1 receptor antagonist, 100 nM, 1 μL), GABA (50 mM, 1 μL) or saline (1 μL) were injected into the mPOA, and the variables were measured for additional 30 min. In a different group of rats, the AT-1 receptor, angiotensin II converting enzyme (ACE), and GABAa receptor gene expression was evaluated in mPOA samples by qPCR. The data are as mean ± SEM and submitted to One-way ANOVA (Tukey posttest) or paired Student t-test (P <0.05). Results: The injection of Ang II into the mPOA evoked a significant hypotension (-37±10 mmHg, n = 6, p = 0.024) and bradycardia (-47 ± 20 bpm, p = 0.030) compared to saline (+1 ± 1 mmHg and +6 ± 2 bpm, n = 6). A significant increase in IP was observed after Ang II injection into the mPOA (+72.25 ± 17.91%, p = 0.015 vs. -1.80 ± 2.98%, n = 6, saline). No significant changes were observed in MAP, HR and IP after the losartan injection in the mPOA compared to saline injection. Injection of GABA into the mPOA evoked a significant fall in MAP and HR (-68 ± 2 mmHg, n = 6, p < 0.0001 and -115 ± 14 bpm, n = 6, p = 0.0002 vs. -1 ± 1 mmHg and +4 ± 2 bpm, n = 6, saline), but no significant changes were observed in IP. The AT-1 receptor, ACE and GABAa receptor mRNA expression was observed in all mPOA samples. Discussion: Therefore, in female rats, Ang II mediated transmission in the mPOA is involved in the cardiovascular regulation and in the control of central
micturition pathways. A phasic control dependent on AT-1 receptors in the mPOA seems to be involved in the regulation of those cardiovascular and intravesical 3 parameters. In contrast, GABAergic transmission in the mPOA participates in the pathways of cardiovascular control in anesthetized female rats, nevertheless, this neurotransmission is not involved in the
micturition control.