The enzyme aldosterone synthase (also known as CYP11B2 ) acts in this location   The expression of neuron-specific proteins in the zona glomerulosa cells of human adrenocortical tissues has been predicted and reported by several authors    and it was suggested that the expression of proteins like the neuronal cell adhesion molecule (NCAM) in the cells of the zona glomerulosa reflects the regenerative feature of these cells, which would lose NCAM immunoreactivity after moving to the zona fasciculata .   However, together with other data on neuroendocrine properties of zona glomerulosa cells, NCAM expression may reflect a neuroendocrine differentiation of these cells.  Voltage-dependent calcium channels have been detected in the zona glomerulosa of the human adrenal, which suggests that calcium-channel blockers may directly influence the adrenocortical biosynthesis of aldosterone in vivo. 
Following heart failure , the body increases sympathetic activity to the adrenal medulla as the compensatory mechanism to increase heart rate and cardiac output . This increased sympathetic activity leads to chronically increased synthesis and secretion of catecholamines from the adrenal chromaffin cells. This chronic increase of epinephrine and norepinephrine secretion causes desensitization of the chromaffin cells to catecholamines resulting in a decrease in production and presence of α 2 adrenergic receptors on their cell membrane. This desensitization and downregulation of α 2 adrenergic receptors is caused by the upregulation of the enzyme Adrenal G protein coupled receptor kinase 2 ( GRK2 ) which effectively eliminates the normal autocrine-type negative feedback that normally prevents the cells from over producing the catecholamines and replaces it with a positive feedback loop in which increased secretion further elicits more secretion.  This upregulation of GRK2 is also accompanied by upregulation and increased production of the enzyme tyrosine hydroxylase , which catalyzes the rate limiting step of catecholamine synthesis. 
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