DIHYDROPYRIDINE-SENSITIVE INITIAL COMPONENT OF THE ANG II-INDUCED CA2+ RESPONSE IN RAT ADRENAL GLOMERULOSA CELLS

The Ca2+ signal induced by an increase in extracellular K+ concentrati on from 3.6 to 5.6 mM or angiotensin II (ANG II) was inhibited by the dihydropyridine (DHP) Ca2+ channel blocker, nifedipine, and enhanced b y the DHP Ca2+ channel agonist, BAY K 8644. The DHP sensitivity ofthe ANG II-induced Ca2+ response was already detectable during the peak ph ase, suggesting that the DHP receptor plays an important role during t he initial phase of ANG II stimulation. K+ and ANG II stimulated a nif edipine-sensitive Mn2+ influx pathway, further promoting the role of a DHP receptor in their mechanism of action. Fluorescent membrane poten tial measurements showed that, in contrast to the rapid depolarization induced by K+, the ANG II-induced depolarization had a lag time of > 30 s. The slow kinetics of depolarization compared with the immediate effect of ANG II on Mn2+ influx and the DHP sensitivity of the initial Ca2+ peak indicates that ANG II initiates the activation of the DHP-s ensitive Ca2+ channel by a mechanism other than depolarization.