Key result
Dihydropyridine calcium antagonists were more effective inhibitors of K+-induced than ANG II-induced aldosterone secretion in isolated calf adrenal glomerulosa cells.
K+ and ANG II mobilize calcium from different sources for stimulus-response coupling in adrenal glomerulosa cells, though plasma membrane calcium channels show similar sensitivity to nitrendipine.
In vitro data on calf cells leave open whether dihydropyridines differentially suppress aldosterone in humans; clinical relevance untested.
The effects of the dihydropyridine calcium antagonists nimodipine, nitrendipine, and nisoldipine were studied on K+-induced and angiotensin II (ANG II)-induced aldosterone secretion from isolated calf adrenal glomerulosa cells. These drugs were more effective inhibitors of K+-induced secretion than ANG II-induced secretion. However, when the ANG II-induced release of intracellular calcium was blocked by prior treatment of cells with dantrolene, then nitrendipine was equally as effective in blocking ANG II- as K+-induced secretion. On the other hand, the dihydropyridine agonist, BAY K8644, was found to enhance K+-induced secretion to a greater extent than ANG II-induced secretion when the latter was studied in either the absence or presence of dantrolene. It is concluded that K+ and ANG II mobilize calcium from different sources for stimulus-response coupling in these cells and that there is no difference in the sensitivity to nitrendipine of the plasma membrane calcium channels operated by these two different agonists.
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Kojima et al. (1984) studied this question. Dihydropyridine calcium antagonists (nimodipine, nitrendipine, nisoldipine) and agonist (BAY K8644) was evaluated on K+-induced and angiotensin II (ANG II)-induced aldosterone secretion. Dihydropyridine calcium antagonists were more effective inhibitors of K+-induced than ANG II-induced aldosterone secretion in isolated calf adrenal glomerulosa cells.
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