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The purpose of the present investigation was therefore to test the hypothesis that 1 AR-mediated stimulation of norepinephrine release involved peripheral, presynaptic auto-receptors, or alternatively, was due to epinephrine secretion, reduced ganglion transmission, or reduced renal renin secretion with subsequent presynaptic AT1R-activation

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Other studies refer to modulation of the gene expression which is involved in the regulation of MAO activity by carotenoids