Li Y W, Guyenet P G
University of Virginia, Department of Pharmacology, Charlottesville 22908, USA.
Circ Res. 1996 Feb;78(2):274-82. doi: 10.1161/01.res.78.2.274.
In the rostral ventrolateral medulla (RVLM), angiotensin II (Ang II) receptors are concentrated in the region that contains neurons innervating sympathetic preganglionic neurons. We sought to determine whether these bulbospinal cells are sensitive to Ang II. Retrogradely labeled bulbospinal RVLM neurons (N = 125) were recorded in thin slices from neonatal rats. Most (33 of 46) histologically recovered bulbospinal neurons were C1 cells (immunoreactive for tyrosine hydroxylase [TH-ir] or phenylethanolamine N-methyltransferase [PNMT-ir]). Bulbospinal RVLM neurons were spontaneously active (2.7 +/- 0.2 spikes per second, n = 69) with 'resting' potential of -54 +/- 0.4 mV (n = 77) and input resistance of 879 +/- 53 M omega (n = 47). Ang II (0.3 to 1 mumol/L) increased the spontaneous firing rate of most bulbospinal neurons (+250%, 28 of 39). In current-clamp mode, Ang II (1 mumol/L) produced depolarization (+6.8 +/- 0.6 mV, n = 59 neurons) and increased input resistance (+21 +/- 2%, n = 36 neurons). In voltage-clamp mode, Ang II elicited an inward current (9.7 +/- 0.9 pA; holding potential, -40 to -55 mV; n = 25 neurons) that reversed polarity at the K+ equilibrium potential (n = 8 neurons) and was barium sensitive (n = 4 neurons). Ang II-evoked conductance change was voltage independent (-40 to -140 mV, n = 8 neurons). The effects of Ang II were blocked by losartan (9 of 9 neurons) but persisted in low Ca2+/high Mg2+ (7 of 7 neurons). Ang II-sensitive cells were inhibited by alpha 2-adrenergic receptor agonists (12 of 15 neurons). Ang II excited 91% (30 of 33) of TH-ir or PNMT-ir cells but 23% (3 of 13) of non-TH-ir neurons. In conclusion, RVLM bulbospinal cells express Ang II type-1 receptors whose activation leads to a reduction in resting K+ conductance.
在延髓头端腹外侧区（RVLM），血管紧张素II（Ang II）受体集中于含有支配交感神经节前神经元的神经元区域。我们试图确定这些延髓脊髓细胞是否对Ang II敏感。在新生大鼠的薄片中记录逆行标记的延髓脊髓RVLM神经元（N = 125）。大多数（46个中的33个）组织学上恢复的延髓脊髓神经元是C1细胞（对酪氨酸羟化酶[TH-ir]或苯乙醇胺N-甲基转移酶[PNMT-ir]免疫反应阳性）。延髓脊髓RVLM神经元自发活动（每秒2.7±0.2个峰电位，n = 69），“静息”电位为-54±0.4 mV（n = 77），输入电阻为879±53 MΩ（n = 47）。Ang II（0.3至1 μmol/L）增加了大多数延髓脊髓神经元的自发放电率（增加250%，39个中的28个）。在电流钳模式下，Ang II（1 μmol/L）产生去极化（+6.8±0.6 mV，n = 59个神经元）并增加输入电阻（+21±2%，n = 36个神经元）。在电压钳模式下，Ang II引起内向电流（9.7±0.9 pA；钳制电位，-40至-55 mV；n = 25个神经元），该电流在K+平衡电位处反转极性（n = 8个神经元）且对钡敏感（n = 4个神经元）。Ang II诱发的电导变化与电压无关（-40至-140 mV，n = 8个神经元）。Ang II的作用被氯沙坦阻断（9个神经元中的9个），但在低钙/高镁环境中持续存在（7个神经元中的7个）。Ang II敏感细胞被α2-肾上腺素能受体激动剂抑制（15个神经元中的12个）。Ang II兴奋了91%（33个中的30个）的TH-ir或PNMT-ir细胞，但只兴奋了23%（13个中的3个）的非TH-ir神经元。总之，RVLM延髓脊髓细胞表达Ang II 1型受体，其激活导致静息K+电导降低。
