Buggy J, Huot S, Pamnani M, Haddy F
Fed Proc. 1984 Jan;43(1):25-31.
Periventricular forebrain regions participate in body fluid and cardiovascular regulatory mechanisms that are intimately related to neural participation in experimental hypertension. Ablation of preoptic-hypothalamic periventricular tissue surrounding the anteroventral third ventricle (AV3V) disrupts both angiotensin (AngII) and sodium regulatory mechanisms and prevents experimental hypertension in either renin-dependent or -independent models. When AV3V is spared, and central AngII pressor mechanisms are interrupted by subfornical organ ablation or anterior hypothalamic knife cuts, renin-dependent but not renin-independent models of hypertension are prevented. Volume-expanded models of hypertension may be mediated by a natriuretic hormone that also inhibits the sodium-potassium pump in vascular smooth muscle, resulting in increased vasoconstriction. Volume expansion-induced release of this humoral ATPase inhibitor is attenuated in rats with AV3V lesions. In the renin-independent, reduced renal mass model, development of hypertension is correlated with increased plasma levels of sodium-potassium pump inhibitor. AV3V ablation blocks both the hypertension and the increase in humoral ATPase inhibitor. Thus, Thus, central angiotensin pressor and natriuretic mechanisms overlap in AV3V, and prevention of renin-dependent and volume-dependent models of experimental hypertension by AV3V ablation appears linked to disruption of these functionally separable systems.
脑室周围的前脑区域参与了体液和心血管调节机制，这些机制与神经因素参与实验性高血压密切相关。切除围绕第三脑室前腹侧（AV3V）的视前 - 下丘脑脑室周围组织，会破坏血管紧张素（AngII）和钠调节机制，并在肾素依赖性或非依赖性模型中预防实验性高血压。当AV3V得以保留，且通过穹窿下器切除或下丘脑前部刀切术中断中枢性AngII升压机制时，肾素依赖性而非肾素非依赖性高血压模型得以预防。高血压的容量扩张模型可能由一种利钠激素介导，该激素也抑制血管平滑肌中的钠钾泵，导致血管收缩增加。在患有AV3V损伤的大鼠中，容量扩张诱导的这种体液ATP酶抑制剂的释放会减弱。在肾素非依赖性、肾质量减少模型中，高血压的发展与钠钾泵抑制剂的血浆水平升高相关。AV3V切除可阻断高血压以及体液ATP酶抑制剂的增加。因此，中枢性血管紧张素升压和利钠机制在AV3V中重叠，并且通过AV3V切除预防肾素依赖性和容量依赖性实验性高血压模型似乎与这些功能上可分离的系统的破坏有关。
