PubMed · 9496359
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Z Blumenfeld. 1998. Provocative testing with ACTH interpretation.. https://doi.org/10.1016/s0015-0282(97)00493-7
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To define the effects of adrenocorticotropic hormone (ACTH) in immunocompetent cells, ion channel activities in cultured mouse peritoneal macrophages were analyzed by the perforated patch-clamp method. ACTH induced outward currents at smaller holding potentials than K+ equilibrium potentials. Reversal potentials of ACTH-induced currents were dependent on external K+ concentrations, but not on external Cl- concentration. Quinine potently blocked the outward current and tetraethylammonium (TEA) partially suppressed that current. ACTH did not induce the response in Ca2+ free solution containing EGTA. These results suggest that ACTH can modulate macrophage functions through the activation of Ca2+ dependent K+ channels.
Recently it was shown that the cholinergic agonist carbachol stimulates cortisol production in bovine ZFR cells via muscarinic receptor M(3). In the present study, we investigated the effect of chronic cholinergic stimulation on steroidogenic response and muscarinic receptor regulation in ZFR cells. Cortisol secretion of ZFR cells treated with 10(-4) M of carbachol decreased in a dose- and time-dependent manner. The carbachol-elicited loss of response was associated with a decrease in M(3) receptor number, which was also time- and dose-dependent. The down-regulation of the receptors was not associated with the decrease of M(3) receptor mRNA level. The marked steroidogenic desensitization caused by pretreatment of carbachol did not alter ACTH or angiotensin II activated steroid response. Northern blot analysis showed that carbachol pretreatment did not change the gene expression of P450scc, P450cl7, 3betaHSD and StAR mRNAs. These results suggest that carbachol induces homologous steroidogenic refractoriness of ZFR cells.
We studied the complex interactions within the neuroendocrine-immune-hematopoietic axis by determining a possible link among ACTH, PRL, PPT-I and the receptors for its peptides, NK-1 and NK-2. Indeed, ACTH and PRL induced the expression of PPT-I and NK-1 in human bone marrow stroma with no effect on NK-2. Consistent with a role for PPT-I in regulating the development of myeloid and erythroid progenitors, we found that ACTH and PRL, through NK-1 stimulated the proliferation of both types of progenitors. Induction of PPT-I was regulated at the transcriptional and post-transcriptional levels. The results showed that ACTH and PRL stimulated the proliferation of bone marrow progenitors, partly through PPT-I and NK-1 induction.