Andreatta-Van Leyen S, Averill D B, Ferrario C M
Department of Brain and Vascular Research, Cleveland Clinic Foundation, Ohio 44195-5070.
Hypertension. 1990 Feb;15(2 Suppl):I102-6. doi: 10.1161/01.hyp.15.2_suppl.i102.
Vasopressin acts at a number of sites in the central nervous system to alter arterial pressure. This study investigated the hypothesis that vasopressin acts at the rostral ventrolateral medulla to increase arterial pressure. The rostral pressor area of the medulla oblongata was exposed in urethane-anesthetized rats prepared for topical application of vasopressin. A 3-minute application of vasopressin (range 10(-8) to 10(-3) M) produced dose-dependent increases in arterial pressure that averaged between 2 +/- 1 and 65 +/- 11 mm Hg (p less than 0.01). Tachycardia was not a consistent response at any concentration of vasopressin. Intravenous administration of a V1 vasopressin antagonist did not modify the pressor response produced by topical application of vasopressin (10(-4) M). Application of the V1 antagonist to the rostral pressor area, however, prevented the production of a pressor effect to subsequent topical application of vasopressin (10(-4) M). These experiments suggest that vasopressin stimulates the activity of vasomotor neurons in the rostral ventrolateral medulla by a mechanism that involves a neuronal V1 receptor.
血管加压素作用于中枢神经系统的多个部位以改变动脉血压。本研究探讨了血管加压素作用于延髓头端腹外侧区以升高动脉血压的假说。在为局部应用血管加压素而制备的经乌拉坦麻醉的大鼠中,暴露延髓头端加压区。局部应用血管加压素(浓度范围为10⁻⁸至10⁻³ M)3分钟,可使动脉血压呈剂量依赖性升高,平均升高幅度在2±1至65±11 mmHg之间(p<0.01)。在任何血管加压素浓度下,心动过速都不是一致的反应。静脉注射V1血管加压素拮抗剂并不会改变局部应用血管加压素(10⁻⁴ M)所产生的升压反应。然而,将V1拮抗剂应用于延髓头端加压区,则可阻止随后局部应用血管加压素(10⁻⁴ M)产生升压效应。这些实验表明,血管加压素通过一种涉及神经元V1受体的机制刺激延髓头端腹外侧区血管运动神经元的活动。