Talman William T, Dragon Deidre Nitschke
Department of Neurology, Laboratory of Neurobiology, VAMC and University of Iowa, Iowa City, IA 52242, USA.
Hypertension. 2004 Apr;43(4):820-4. doi: 10.1161/01.HYP.0000120848.76987.ef. Epub 2004 Feb 23.
Because inhibition of neuronal nitric oxide synthase in the nucleus tractus solitarii blocks cardiovascular responses to activation of local glutamate receptors, and because glutamate is a neurotransmitter of baroreceptor afferent nerves, we sought to test the hypothesis that neuronal nitric oxide synthase inhibition would block baroreflex transmission and cause hypertension. We determined reflex heart rate responses to intravenous phenylephrine and sodium nitroprusside in 5 anesthetized rats before and after bilateral microinjection (100 nL) of the neuronal nitric oxide synthase inhibitor AR-R 17477 (7.5 nmol) into the nucleus tractus solitarii. The inhibitor significantly increased mean arterial pressure without affecting heart rate, and it significantly reduced the gain of the baroreflex. After administration of the inhibitor, reflex responses of heart rate to changes in mean arterial pressure were always less than those responses to the same, or less, change in mean arterial pressure in the same animal without administration of the inhibitor. Microinjection of saline (100 nL) bilaterally into the nucleus tractus solitarii did not lead to hypertension or change baroreflex responses. These data support the hypothesis and suggest that neuronal nitric oxide synthase is critical to transmission of baroreflex signals through the nucleus tractus solitarii.
由于孤束核中神经元型一氧化氮合酶的抑制会阻断对局部谷氨酸受体激活的心血管反应，且由于谷氨酸是压力感受器传入神经的一种神经递质，我们试图检验神经元型一氧化氮合酶抑制会阻断压力感受性反射传导并导致高血压这一假说。我们在5只麻醉大鼠双侧微量注射（100 nL）神经元型一氧化氮合酶抑制剂AR-R 17477（7.5 nmol）至孤束核前后，测定了对静脉注射去氧肾上腺素和硝普钠的反射性心率反应。该抑制剂显著升高平均动脉压而不影响心率，且显著降低压力感受性反射的增益。给予抑制剂后，心率对平均动脉压变化的反射反应总是小于同一动物在未给予抑制剂时对相同或更小的平均动脉压变化的反应。双侧向孤束核微量注射生理盐水（100 nL）未导致高血压或改变压力感受性反射反应。这些数据支持该假说，并表明神经元型一氧化氮合酶对于压力感受性反射信号通过孤束核的传导至关重要。
