Regulation of angiotensin II receptors in the rat adrenal cortex by dietary electrolytes.
Regulation of angiotensin II receptors in the rat adrenal cortex by dietary electrolytes.
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膳食电解质对大鼠肾上腺皮质血管紧张素 II 受体的调节。
DOI：
10.1172/jci108536
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发表时间：
1976
期刊：
影响因子：
--
通讯作者：
K. Catt
中科院分区：
文献类型：
--
作者：
J. Douglas;K. Catt
大鼠肾上腺皮质细胞和匀浆的特异性血管紧张素II受体位点的结合亲和力和浓度的测定后1和6周的改变钠和钾的摄入量。钠剥夺引起血浆肾素、血液血管紧张素II和血浆醛固酮显著增加，并伴随着每个肾上腺皮质细胞特异性血管紧张素II受体位点数量的显著增加（+74%）。高钾摄入量增加，血清钾和血浆醛固酮显着升高，与低于正常水平的肾素和血管紧张素II和血管紧张素II受体的数量增加170%，每个细胞后1周。钠负荷和钾剥夺后，肾上腺受体的相反的效果，减少血管紧张素II结合能力。没有饮食电解质的变化伴随着受体亲和力高于2 nM-1的控制值的增加。低钠或低钾摄入6周后，当肾素和血管紧张素II水平增加104- 129%时，受体亲和力下降。用合成的血管紧张素II急性注入正常大鼠的肾上腺，或用乙醚或戊巴比妥钠麻醉的正常大鼠的肾上腺，其显著增加血浆肾素活性，含有较少的血管紧张素受体。这些结合位点浓度的降低并不伴随着亲和力的变化，并归因于血管紧张素II的占用。这些研究表明，钠或钾平衡的慢性变化和血液血管紧张素II水平的急性变化可对肾上腺含量和/或血管紧张素II特异性受体位点的亲和力产生调节作用。
The binding affinity and concentration of specific angiotensin II receptor sites of rat adrenal cortical cells and homogenates were determined after 1 and 6 wk of altered sodium and potassium intake. Sodium deprivation caused marked increases in plasma renin, blood angiotensin II, and plasma aldosterone, and was accompanied by a significant increase (+74%) in the number of specific angiotensin II receptor sites per adrenal cortical cell. High potassium intake was followed by increased serum potassium and markedly elevated plasma aldosterone, with subnormal levels of renin and angiotensin II and a 170% increase in the number of angiotensin II receptors per cell after 1 wk. Sodium loading and potassium deprivation were followed by the opposite effect upon adrenal receptors, with reduction of the angiotensin II-binding capacity. None of the dietary electrolyte changes were accompanied by an ancrease in receptor affinity above the control value of 2 nM-1. A decrease in receptor affinity was noted after 6 wk of either low sodium or low potassium intake, when the renin and angiotensin II levels were increased by 104-129%. The adrenals of normal rats infused acutely with synthetic angiotensin II, or anesthetized with ether or sodium pentobarbital, which markedly increased plasma renin activity, contained fewer angiotensin receptors. These reductions in binding site concentration were not accompanied by changes in affinity and were attributed to occupancy by angiotensin II. These studies have demonstrated that chronic changes in sodium or potassium balance and acute changes in blood angiotensin II levels can exert modulating effects upon the adrenal content and/or affinity of specific receptor sites for angiotensin II.