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钠负荷导致血压升高和增加血管反应性的机理,目前多倾向于接受Folkow的外周阻力取决于血管壁(厚度)/腔(半径)的公式。因钠的滞留使血管壁中层水肿、管腔减小,从而升高外周阻力并对缩血管活性物质产生较强的收缩。近年研究证明钙离子的膜内外转运是平滑肌收缩的基础并与高血压发生有密切关系。本工作通过硝苯吡啶阻断钙通道,探讨钠负荷大鼠血管反应性和钙的关系。
The mechanism by which sodium load leads to increased blood pressure and increased vascular reactivity is now mostly inclined to accept the fact that the peripheral resistance of Folkow depends on the formula of the vessel wall (thickness) / lumen (radius). Because of sodium retention of the middle of the vessel wall edema, lumen decreased, thereby increasing peripheral resistance and vasoconstrictor active substances have a stronger contraction. In recent years, studies have shown that calcium ion transport inside and outside the membrane is the basis of smooth muscle contraction and hypertension are closely related. This work through the nifedipine block calcium channel, to explore the relationship between vascular reactivity and calcium in sodium-loaded rats.