Regulation of Vascular Angiotensin II Receptors in the Rat during Altered Sodium Intake
Regulation of Vascular Angiotensin II Receptors in the Rat during Altered Sodium Intake
复制标题
改变钠摄入量时大鼠血管血管紧张素 II 受体的调节
作者：
G. Aguilera;K. Catt
钠摄入量的变化对肾上腺和血管对血管紧张素n的反应性产生明确和相反的影响（所有）。而肾上腺小球区变得更敏感的所有在限钠期间，血管的敏感性下降，钠限制和增加钠负荷。在多大程度上调节平滑肌的所有受体参与这种改变血管反应性的测定125 I-AU结合在肠系膜动脉和膀胱的大鼠在低和高钠摄入量。血管平滑肌的所有受体被认为是类似的肠系膜动脉的结合特性和调节改变钠摄入量方面。在限钠期间，两种组织中的血液All升高，All受体浓度显著降低（40%）。相反，钠负荷伴随着血液中的所有减少和平滑肌所有受体的增加。钠限制期间所有结合的变化不归因于内源性An对受体的占用，并且在钠摄入的任一极端均未观察到对受体亲和力的影响。通过输注八肽2-4天，在生理范围内升高循环AD浓度，可降低膀胱颗粒中的An受体浓度。这些研究结果表明，平滑肌的所有受体的调节过程中改变钠的摄入量，至少部分地通过在循环中的所有浓度的变化，在肾上腺肾小球受体的方式相互作用。血管AH受体的这种调节可能是由于伴随钠平衡变化的升压反应改变和循环中高水平ALL患者血管反应性降低所致。
Changes in sodium intake exert well-defined and opposite effects on adrenal and vascular responsiveness to angiotensin n (All). Whereas the adrenal glomerulosa zone becomes more sensitive to All during sodium restriction, vascular sensitivity to All is decreased during sodium restriction and increased by sodium loading. The extent to which regulation of smooth muscle All receptors is involved in such altered vascular responsiveness was examined by assay of 125I-AU binding in the mesenteric artery and urinary bladder of rats during low and high sodium intake. The All receptors of vascular smooth muscle were found to be similar to those of the mesenteric artery in terms of their binding properties and regulation by altered sodium intake. During sodium restriction, blood All was elevated and All receptor concentration was significantly decreased (by 40%) in both tissues. Conversely, sodium loading was accompanied by decreased blood All and an increase in smooth muscle All receptors. The changes in All binding during sodium restriction were not attributable to occupancy of receptors by endogenous An, and no effect on receptor affinity was observed at either extreme of sodium intake. Elevation of the circulating AD concentration within the physiological range by infusion of the octapeptide for 2–4 days decreased An receptor concentration in urinary bladder particles. These findings demonstrate that smooth muscle All receptors are regulated during altered sodium intake, at least partially via changes in the circulating All concentration, in a manner reciprocal to the adrenal glomerulosa receptors. Such modulation of vascular AH receptors by the renin-angiotensin system could be responsible both for the altered pressor responses that accompany changes in sodium balance and for the reduced vascular reactivity that occurs in patients with high levels of circulating All.