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Taeyoon Kim, Y. Peng Loh
Published in Volume 115, Issue 7
J Clin Invest. 2005; 115(7):1711–1713 doi:10.1172/JCI25706
Abstract | Full text | PDF
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Figure 1

Relationship of CHGA-mediated dense-core secretory granule (DCG) biogenesis, catecholamine (CA) secretion, and its subsequent inhibition by the CHGA-derived peptide catestatin in the maintenance of blood pressure by the adrenal gland. CHGA, as a full-length molecule, initiates dense-core secretory granule biogenesis at the trans-Golgi network of adrenal chromaffin cells. Current data suggests that CHGA enhances granule biogenesis by preventing posttranslational degradation of other granule proteins in the Golgi complex. In the cytoplasm, catecholamine is synthesized and transported into the dense-core secretory granules via vesicular monoamine transporters. Upon stimulation by acetylcholine (Ach), catecholamine is coreleased with CHGA and catestatin from the granules. Secreted catecholamine triggers cardiovascular target cells to augment blood flow. This sympathoadrenal activity is then antagonized by the action of catestatin on cholinergic receptors to inhibit catecholamine secretion. [Ca2+]i, intracellular calcium concentration.