Schiebinger R J
J Clin Invest. 1985 Dec;76(6):2165-70. doi: 10.1172/JCI112223.
Angiotensin II-stimulated secretion by adrenal glomerulosa cells and contraction by vascular smooth muscle (VSM) are dependent on calcium influx through membrane calcium channels. We have examined the hypothesis that the altered responsiveness of adrenal glomerulosa cells and VSM to angiotensin II during NaCl restriction may be associated with a change in membrane calcium channel number. To test this hypothesis, female rats were placed on a high or low NaCl diet. On the 14th day, membranes were prepared from the zona glomerulosa, aorta, mesenteric artery, and uterus. [3H]Nitrendipine binding was used to monitor calcium channel number. The [3H]nitrendipine binding capacity was observed to be higher in the zona glomerulosa during NaCl restriction than during high NaCl intake (83 +/- 18 vs. 49 +/- 9 fmol/mg protein, P less than 0.025, n = 6 paired experiments). The binding capacities of [3H]nitrendipine on the low and high NaCl diet were similar in the mesenteric artery (10 +/- 1 vs. 9 +/- 1 fmol/mg protein, n = 8), aorta (33 +/- 5 vs. 35 +/- 8 fmol/mg protein, n = 5), or uterus (87 +/- 15 vs. 85 +/- 16 fmol/mg protein, n = 4), respectively. The dissociation constants of [3H]nitrendipine binding did not differ on a low or high NaCl intake in the zona glomerulosa (0.84 +/- .12 vs. 0.79 +/- .10 nM), mesenteric artery (0.82 +/- .06 vs. 83 +/- .05 nM), aorta (0.90 +/- .11 vs. 0.92 +/- .12 nM), or uterus (0.55 +/- .12 vs. 0.56 +/- .10 nM), respectively. We conclude that the blunted response of VSM to angiotensin II during NaCl restriction is best explained by the previously reported lower number of angiotensin II receptors since calcium channel number does not change. In the adrenal glomerulosa cell, NaCl restriction is associated with a higher number of membrane calcium channels and angiotensin II receptors. The increase in calcium channel number may reflect the influence of an unknown factor(s) believed to be necessary for the full expression of the adrenal glomerulosa cell response to NaCl restriction.
血管紧张素II刺激肾上腺球状带细胞分泌以及引起血管平滑肌（VSM）收缩均依赖于通过膜钙通道的钙内流。我们检验了这样一个假说：在限盐期间肾上腺球状带细胞和VSM对血管紧张素II反应性的改变可能与膜钙通道数量的变化有关。为验证这一假说，将雌性大鼠置于高盐或低盐饮食。在第14天，从球状带、主动脉、肠系膜动脉和子宫制备细胞膜。用[3H]尼群地平结合法监测钙通道数量。观察到限盐期间球状带中[3H]尼群地平的结合能力高于高盐摄入期间（83±18对49±9 fmol/mg蛋白质，P<0.025，n=6对实验）。低盐和高盐饮食时[3H]尼群地平在肠系膜动脉（10±1对9±1 fmol/mg蛋白质，n=8）、主动脉（33±5对35±8 fmol/mg蛋白质，n=5）或子宫（87±15对85±16 fmol/mg蛋白质，n=4）中的结合能力分别相似。[3H]尼群地平结合的解离常数在低盐或高盐摄入时在球状带（0.84±0.12对0.79±0.10 nM）、肠系膜动脉（0.82±0.06对0.83±0.05 nM）、主动脉（0.90±0.11对0.92±0.12 nM）或子宫（0.55±0.12对0.56±0.10 nM）中并无差异。我们得出结论，限盐期间VSM对血管紧张素II反应减弱最好用先前报道的血管紧张素II受体数量减少来解释，因为钙通道数量没有变化。在肾上腺球状带细胞中，限盐与更多的膜钙通道和血管紧张素II受体相关。钙通道数量的增加可能反映了一种未知因子的影响，该因子被认为是肾上腺球状带细胞对限盐充分反应所必需的。
