Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Iseigaoka, Yahatanishiku, Kilakyushu 807, Japan.
J Neuroendocrinol. 1991 Feb 1;3(1):45-9. doi: 10.1111/j.1365-2826.1991.tb00237.x.
Abstract It is not entirely clear whether or not atrial natriuretic peptide (ANP) directly inhibits vasopressin neurons in the supraoptic nucleus (SON) and paraventricular nucleus. Recently, a novel peptide, brain natriuretic peptide (BMP), which has been isolated from the brain, has been shown to have a similar action to ANP on the regulation of vasopressin release. Intracerebroventricular injection of both BNP and ANP inhibits stimulus-evoked increases of plasma vasopressin level. The present study was undertaken: 1) to investigate whether BNP affects the activity of neurons in the region of the anteroventral third ventricle (AV3V) and SON which are involved in the control of body fluid homeostasis and blood pressure regulation, 2) to reassess effects of ANP on SON neurons, and 3) to test whether BNP exerts its effects by mechanisms which are different from those of ANP. Extracellular recordings were made from 213 AV3V and 110 SON spontaneously firing neurons in the rat coronal hypothalamic slice preparation. Of the AV3V neurons tested, BNP inhibited 86 (40%) and excited 2 (1%) while 125 neurons remained unaffected. A dose-response relationship was obtained for 7 AV3V neurons at different BNP concentrations ranging from 10(-11) M to 10(-6) M; the firing rates of all 7 neurons decreased. The threshold concentration to evoke inhibitory responses was approximately 10(-10)M in the AV3V. When BNP and ANP were applied to the same neuron, most AV3V neurons which were inhibited by BNP were also inhibited by ANP and the neurons which were unaffected by BNP were also unaffected by ANP. Thus, these two peptides probably have a similar action on AV3V neurons. When BNP and angiotensin II were applied to a group of 60 neurons in the AV3V, most of the responsive neurons showed either inhibitory responses to BNP or excitatory responses to angiotensin II. Both BNP and ANP were applied to a group of 110 SON neurons: BNP (10 (-7) M) inhibited 52 (75%) of 69 phasic (putative vasopressin) neurons, while BNP affected none of the 41 non-phasic (putative oxytocin) neurons. By contrast, ANP inhibited only 20 (29%) of 69 phasic neurons tested but it also had no effect on 41 non-phasic neurons tested. Our results are consistent with the suggestion that BNP is involved in the regulation of vasopressin release by acting on SON neurons and AV3V neurons.
目前尚不清楚心房利钠肽（ANP）是否直接抑制视上核（SON）和室旁核中的血管加压素神经元。最近，一种从脑中分离出来的新型肽——脑利钠肽（BMP），已被证明在调节血管加压素释放方面与 ANP 具有相似的作用。脑室内注射 BNP 和 ANP 均可抑制刺激引起的血浆血管加压素水平升高。本研究旨在：1）探讨 BNP 是否影响参与体液稳态和血压调节的前腹第三脑室（AV3V）和 SON 区域中神经元的活动；2）重新评估 ANP 对 SON 神经元的影响；3）测试 BNP 是否通过与 ANP 不同的机制发挥作用。在大鼠冠状下丘脑切片制备中，从 213 个 AV3V 和 110 个 SON 自发放电神经元中进行了细胞外记录。在测试的 AV3V 神经元中，BNP 抑制了 86 个（40%），兴奋了 2 个（1%），而 125 个神经元不受影响。在 7 个 AV3V 神经元中，在不同的 BNP 浓度范围内（从 10(-11)M 到 10(-6)M）获得了剂量反应关系；7 个神经元的放电率均下降。在 AV3V 中，引起抑制反应的阈浓度约为 10(-10)M。当 BNP 和 ANP 应用于同一神经元时，大多数被 BNP 抑制的 AV3V 神经元也被 ANP 抑制，而不受 BNP 影响的神经元也不受 ANP 影响。因此，这两种肽可能对 AV3V 神经元具有相似的作用。当 BNP 和血管紧张素 II 应用于 AV3V 中的一组 60 个神经元时，大多数有反应的神经元对 BNP 表现出抑制反应，对血管紧张素 II 表现出兴奋反应。BNP 和 ANP 均应用于一组 110 个 SON 神经元：BNP（10(-7)M）抑制了 69 个相位（推定的血管加压素）神经元中的 52 个（75%），而 BNP 对 41 个非相位（推定的催产素）神经元无影响。相比之下，ANP 仅抑制了 69 个相位神经元中测试的 20 个（29%），但对 41 个非相位神经元也没有影响。我们的结果与 BNP 通过作用于 SON 神经元和 AV3V 神经元参与血管加压素释放调节的观点一致。
