Haywood J R, Brennan T J, Hinojosa C
Fed Proc. 1985 May;44(8):2393-9.
The contribution of neurohumoral factors to arterial pressure has been studied in several models of sodium-dependent hypertension including the deoxycorticosterone-saline, Dahl salt-sensitive rats, and reduced renal mass-saline. Observations from these animals have largely pointed to the sympathetic nervous system and arginine vasopressin (AVP) as the critical factors responsible for mediating the increased arterial pressure. Our work has indicated that the one-kidney, figure-8 renal wrap model of experimental hypertension is also sodium dependent. In these rats, prior sodium depletion prevented the development of hypertension whereas high sodium intake exacerbated the increase in arterial pressure. An activation of the sympathetic nervous system and increased AVP activity appeared to be responsible for the hypertension in rats maintained on normal and high sodium intake. Stimulation of the AVP and sympathetic nervous systems in sodium-dependent hypertension may be associated with a suppression of cardiovascular gamma-aminobutyric acid (GABA)-ergic function in the central nervous system. The inhibitory neurotransmitter, GABA, and an inhibitor of GABA uptake, nipecotic acid, lowered arterial pressure in a sodium-stimulated model of hypertension.
在多种钠依赖性高血压模型中，包括脱氧皮质酮-生理盐水模型、 Dahl盐敏感大鼠模型和肾质量减少-生理盐水模型，已经对神经体液因素对动脉血压的作用进行了研究。对这些动物的观察结果大多表明，交感神经系统和精氨酸加压素（AVP）是介导动脉血压升高的关键因素。我们的研究表明，实验性高血压的单肾、8字形肾包裹模型也是钠依赖性的。在这些大鼠中，预先的钠耗竭可预防高血压的发展，而高钠摄入则会加剧动脉血压的升高。交感神经系统的激活和AVP活性的增加似乎是维持正常和高钠摄入的大鼠发生高血压的原因。在钠依赖性高血压中，AVP和交感神经系统的刺激可能与中枢神经系统中心血管γ-氨基丁酸（GABA）能功能的抑制有关。抑制性神经递质GABA和GABA摄取抑制剂哌啶酸在钠刺激的高血压模型中可降低动脉血压。
