By Bernard L. Horecker, Earl R. Stadtman, P. Boon Chock
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Additional info for Current topics in cellular regulation / 31
Therefore no activation of protein kinase C occurs, and there is no increase in the extent of phosphorylation of the late-phase proteins (Pr bP). Hence no sustained increase in aldosterone secretory rate is observed. 52 HOWARD RASMUSSEN AND JANE E. RASMUSSEN is a direct consequence of hormone-receptor interaction and is indepen2 + 2+ dent of C a . However, in many cell types both C a - d e p e n d e n t and 2+ C a - i n d e p e n d e n t forms of PI-PLC exist, as does clear evidence t h a t both play a role in an agonist-induced response.
As a consequence, there is a 2+ 2+ compensatory increase in C a efflux rate so t h a t [ C a ] i falls back to its original value and, throughout the remainder of the response, there 2+ is an increase in C a cycling across the plasma membrane without a 2+ net gain in total cell calcium. The duration of the [ C a ] i transient is a 2+ measure of the rapidity with which the increase in C a influx rate leads to a compensatory increase in efflux rate: approximately 15 sec in 2+ a mixed cell population.
The increase in C a influx rate produced by Ang II is additive to t h a t produced by ACTH, implying t h a t the ACTH2+ induced C a entry occurs by a different pathway t h a t then acted on by Ang II. This conclusion is supported by the finding t h a t nitrendipine 2+ blocks Ang II but not ACTH-induced C a entry. From these data, a model of ACTH action has been developed in 2+ which C a and cAMP serve as coordinate messengers. ACTH, via one 2+ receptor class, stimulates C a entry and, via another receptor class, 2 + adenylate cyclase.
Current topics in cellular regulation / 31 by Bernard L. Horecker, Earl R. Stadtman, P. Boon Chock