Sanchez P, Damase-Michel C, Tran M A, Montastruc J L
Laboratoire de Pharmacologie Médicale et Clinique, INSERM U 317, Faculté de Médecine, Toulouse, France.
Hypertens Res. 1995 Jun;18 Suppl 1:S187-90. doi: 10.1291/hypres.18.supplementi_s187.
The effect of chronic salt loading (10 g of NaCl for a period of 7 days) on urinary dopamine release has been investigated in 3 groups of beagle dogs: normotensive dogs (group 1: n = 7), and 2 groups of dogs made hypertensive by chronic sinoaortic denervation [group 2: (n = 6) during the first 4 months after sinoaortic denervation i.e. a model of arterial hypertension with high levels of plasma catecholamines and group 3: (n = 6) one year after denervation i.e. a model of arterial hypertension with normal sympathetic tone]. In normal dogs (group 1), salt loading induced an increase in urinary dopamine excretion during the two first days after salt loading. The rise in urinary dopamine was blunted in group 2. It was not observed in group 3. Salt loading failed to change arterial pressure and heart rate in the three groups of animals. These data show an alteration of the renal dopaminergic system in hypertensive sinoaortic denervated dogs suggesting that a dopaminergic impairment can appear during the development of arterial neurogenic hypertension.
研究了慢性盐负荷(7天内给予10克氯化钠)对3组比格犬尿多巴胺释放的影响:正常血压犬(第1组:n = 7),以及2组通过慢性窦主动脉去神经支配制成高血压的犬 [第2组:(n = 6)在窦主动脉去神经支配后的前4个月,即血浆儿茶酚胺水平高的动脉高血压模型;第3组:(n = 6)去神经支配1年后,即交感神经张力正常的动脉高血压模型]。在正常犬(第1组)中,盐负荷在盐负荷后的前两天导致尿多巴胺排泄增加。第2组尿多巴胺的升高减弱。第3组未观察到这种情况。盐负荷未能改变三组动物的动脉血压和心率。这些数据表明高血压窦主动脉去神经支配犬的肾多巴胺能系统发生改变,提示在动脉神经源性高血压的发展过程中可能出现多巴胺能损害。