Modulation der renalen Transmitter-Freisetzung durch präsynaptische Rezeptoren

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Abstract
Renal sympathetic nerve varicosities possess a variety of receptors which when activated by appropriate agonists can modulate noradrenaline release at the local level of the kidney. Thus, activation of prejunctional α1- and α2-adrenoceptors, prostaglandin (PG), dopamine, adenosine and serotonin receptors inhibits, whereas activation of prejunctionalβ2-adrenoceptors and angiotensin (A) II receptors enhances renal noradrenaline release. Moreover, neuronally released noradrenaline itself activates prejunctional inhibitory α1- and α2-adrenoceptors forming a “negative feedback loop” of its own release (autoinhibition). PGE2 and adenosine locally formed in the kidney by renal nerve stimulation inhibits noradrenaline release through activation of their specific prejunctional receptor system (transjunctional inhibition).